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13 minutes ago, iNow said:

How much is that?

 

This is remedially false. There are multiple lines of research showing the ways elderly folks losing memory compensate via other means and through use of mechanisms normally applied elsewhere. Emotion takes on a far greater role too, and reptilian portions of the brain regain much of the lost dominance they had shortly after birth.

 

Perhaps with YOUR current knowledge, but not with mine. Mine would say, details matter here. Incapacitated how, where, and when as obvious followup queries.

We would have to dig much deeper to get to the bottom of this. However, I, at least, and some others in the field find it particularly interesting that a man with such a deficiency is able to even function in the world.

i do not challenge that AD can adapt; i am only saying that in terminal lucidity where going from highly dysfunctional to almost fully functional in a matter of moments, appears to not involve adaptation.

i should have said with the prevailing theories of brain, functional specialization, theory of chemical transmission, neuronal connection, etc. 

1 minute ago, Luc Turpin said:

We would have to dig much deeper to get to the bottom of this. However, I, at least, and some others in the field find it particularly interesting that a man with such a deficiency is able to even function in the world.

i do not challenge that AD can adapt; i am only saying that in terminal lucidity where going from highly dysfunctional to almost fully functional in a matter of moments, appears to not involve adaptation.

i should have said with the prevailing theories of brain, functional specialization, theory of chemical transmission, neuronal connection, etc. 

I am having issues with my computer, who sent this reply without it being verified. Sorry!

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On 12/24/2023 at 8:37 AM, Luc Turpin said:

 

 

I admit to have read too much into the data. So much so that I forgot about the man having only a thin sheet of actual brain with a 75/100 IQ, a job, family and normal life, which concurs with your perspective that continued functionality is maintained in damaged brains. You also present hydrocephaly, leucotomy and other conditions as additional examples of maintained functionality.

 

Nonetheless, how does a man with a large part of his brain missing maintain almost full functionality and lucidity? Or how does an AD patient with significant brain atrophy, widespread damage, neuronal death and severed neuronal connections between various brain regions suddenly recover almost full functionality and lucidity? Other examples given raise similar issues. At play here is the role of brain size, specialized brain areas, neuronal count and neuronal connections on cognition. 
 

The brain may be trying to return to an homeostatic state through neuroplasticity in all of the stated examples, but it may be far from the full picture. Something else might also be at work. Findings like these call into question our conviction of knowing with quasi certainty how our brains work.

Happy holidays!

The crux of your inquiry here appears to question how a brain with severely degraded structure produces behaviors that suggest full functionality and lucidity.  The answer to that requires a cohesive and cogent understanding of brain function by way of its functional evolution.  My understanding of evolution informed me that the functionality of recent brain components is dependent on the function of earlier components and that the function of those early brain components was enhanced by those that emerged recently in brain development.

From my perspective of brain evolution, functionality developed along a clear contiguous path from components that appear to engage primitive functions to those that seem more evolved in their functionality.  To answer the question of functional plasticity in a severely degraded brain, let’s begin with the thalamus.

Most researchers regard the thalamus as a primitive brain structure relative to the neocortex. This suggests that the functionality of the neocortex likely developed after the functional development of the thalamus and that neocortical function is dependent on thalamic function for that reason—the neocortex can’t do what it does for our cognition without a fully functional thalamus as its base.

From my perspective of evolution, recent developments build upon and enhance the efficiency of earlier developments.  Evolution doesn’t necessarily discard primitive developments, but rather build upon and enhance those that are successful.  If that’s true, then our neocortex somehow builds upon and enhances the functionality of the thalamus—but how?

If we agree that the thalamus is our brain’s focal (hub) for sensory input (afference), integration, and output (efference) of our responses to sensory input, we should agree that neocortical function builds upon and enhances what our thalamus does for brain function—that’s if we accept the tenets of evolutional development as I’ve provided.

If our thalamus is a focal for processing (integration) afference and engaging efferently focused behaviors, what might the thalamus need to enhance that function? The answer is likely to be memory as it adds precision to our behaviors.  Next to comparing the relative nature and impact of our sensory experiences (integration), memory is perhaps most important because it allows us to mediate our behavioral responses according to our recall of past sensory experiences—Essentially, memory allows us to learn from our experiences.  This type of mediation would have been essential to the survival of ancestral animals because it would likely have allowed them to conserve their energetic responses to only that stimulus of survival significance.  Memory, among other things, allows us to mediate our behavioral responses to stimuli we’ve learned about and know not to be of significant impact on our experiences and that, at a minimum, is how neocortical function enhances thalamic function.

More precisely, neocortical function allows us to engage in precise behavioral responses relative to our current sensory experiences based on our prior experiences.  Our thalamus has adapted the neocortex as a kind of thinking cap or an extended workspace where the thalamus may attenuate its processing of sensory data.  Regarding plasticity with degraded neocortical structures, clearly a fully functional thalamus that has adapted to limited workspace doesn’t need as much neocortical structure to attenuate its processing as a healthy brain might require.  A functional thalamus in a healthy brain that has suffered severe degeneration requires time to adapt if it does at all within that compromised neural environment.  Resiliency and lucidity is likely dependent on our thalamus’ ability to adapt to its compromised neural environment.

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On 12/25/2023 at 12:49 PM, DrmDoc said:

The crux of your inquiry here appears to question how a brain with severely degraded structure produces behaviors that suggest full functionality and lucidity.  The answer to that requires a cohesive and cogent understanding of brain function by way of its functional evolution.  My understanding of evolution informed me that the functionality of recent brain components is dependent on the function of earlier components and that the function of those early brain components was enhanced by those that emerged recently in brain development.

From my perspective of brain evolution, functionality developed along a clear contiguous path from components that appear to engage primitive functions to those that seem more evolved in their functionality.  To answer the question of functional plasticity in a severely degraded brain, let’s begin with the thalamus.

Most researchers regard the thalamus as a primitive brain structure relative to the neocortex. This suggests that the functionality of the neocortex likely developed after the functional development of the thalamus and that neocortical function is dependent on thalamic function for that reason—the neocortex can’t do what it does for our cognition without a fully functional thalamus as its base.

From my perspective of evolution, recent developments build upon and enhance the efficiency of earlier developments.  Evolution doesn’t necessarily discard primitive developments, but rather build upon and enhance those that are successful.  If that’s true, then our neocortex somehow builds upon and enhances the functionality of the thalamus—but how?

If we agree that the thalamus is our brain’s focal (hub) for sensory input (afference), integration, and output (efference) of our responses to sensory input, we should agree that neocortical function builds upon and enhances what our thalamus does for brain function—that’s if we accept the tenets of evolutional development as I’ve provided.

If our thalamus is a focal for processing (integration) afference and engaging efferently focused behaviors, what might the thalamus need to enhance that function? The answer is likely to be memory as it adds precision to our behaviors.  Next to comparing the relative nature and impact of our sensory experiences (integration), memory is perhaps most important because it allows us to mediate our behavioral responses according to our recall of past sensory experiences—Essentially, memory allows us to learn from our experiences.  This type of mediation would have been essential to the survival of ancestral animals because it would likely have allowed them to conserve their energetic responses to only that stimulus of survival significance.  Memory, among other things, allows us to mediate our behavioral responses to stimuli we’ve learned about and know not to be of significant impact on our experiences and that, at a minimum, is how neocortical function enhances thalamic function.

More precisely, neocortical function allows us to engage in precise behavioral responses relative to our current sensory experiences based on our prior experiences.  Our thalamus has adapted the neocortex as a kind of thinking cap or an extended workspace where the thalamus may attenuate its processing of sensory data.  Regarding plasticity with degraded neocortical structures, clearly a fully functional thalamus that has adapted to limited workspace doesn’t need as much neocortical structure to attenuate its processing as a healthy brain might require.  A functional thalamus in a healthy brain that has suffered severe degeneration requires time to adapt if it does at all within that compromised neural environment.  Resiliency and lucidity is likely dependent on our thalamus’ ability to adapt to its compromised neural environment.

I do not contest the validity of any of the affirmation in your referenced text. Written with clarity and conciseness. We also agree that “the crux of my inquiry appears to question how a brain with severely degraded structure produces behaviors that suggest full functionality and lucidity”. Upon reading and re-reading carefully your text, I remain unconvinced that a brain evolution-plasticity perspective and current understanding of brain function can explain terminal lucidity in Alzheimer’s patients for example. In the context of imminent death, at the highest point of AD degradation, barely maintaining life, being unresponsive prior to lucidity, with numerous brain areas affected and dysfunctional repair systems, the brain is able to almost suddenly mount a late-minute surge to near normal functionality lasting for a few hours or more then suddenly extinguish itself as quickly as it came into being and, all this, just in time for death. I investigated what happens to an AD brain. Most if not all brain regions are irreversibly affected at the end-stage of the disease: neocortex, limbic system, hippocampus, thalamus, hypothalamus, corpus callosum, cerebellum, even the brain stem. Other hallmarks of AD are severe brain shrinkage, plaques and tangles blocking communication, severed neuronal connections, cell death, fibrous astrocytes, axonal swelling and transport disruptions, dysregulation of homeostatic firing and synaptic plasticity, disruption in brain wave pattern, rampant inflammation, major metabolic changes, etc. I reiterate, within the context described above, including the effects of multiple impacts of end-stage AD on the brain, how can it (the brain) even be able to temporarily mount a very-very fast broad-span adaptation and almost full reboot of itself, do so with severely damaged hardware and software, and then go completely off-line before dying? You believe that current knowledge explains terminal lucidity and I do not. To me, something is amiss. However, that we have divergent views on this matter is a suitable “état de fait”. Finally, I will be taking a respite from posting as I have other duties to attend.

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On 12/27/2023 at 6:49 PM, Luc Turpin said:

I do not contest the validity of any of the affirmation in your referenced text. Written with clarity and conciseness. We also agree that “the crux of my inquiry appears to question how a brain with severely degraded structure produces behaviors that suggest full functionality and lucidity”. Upon reading and re-reading carefully your text, I remain unconvinced that a brain evolution-plasticity perspective and current understanding of brain function can explain terminal lucidity in Alzheimer’s patients for example. In the context of imminent death, at the highest point of AD degradation, barely maintaining life, being unresponsive prior to lucidity, with numerous brain areas affected and dysfunctional repair systems, the brain is able to almost suddenly mount a late-minute surge to near normal functionality lasting for a few hours or more then suddenly extinguish itself as quickly as it came into being and, all this, just in time for death. I investigated what happens to an AD brain. Most if not all brain regions are irreversibly affected at the end-stage of the disease: neocortex, limbic system, hippocampus, thalamus, hypothalamus, corpus callosum, cerebellum, even the brain stem. Other hallmarks of AD are severe brain shrinkage, plaques and tangles blocking communication, severed neuronal connections, cell death, fibrous astrocytes, axonal swelling and transport disruptions, dysregulation of homeostatic firing and synaptic plasticity, disruption in brain wave pattern, rampant inflammation, major metabolic changes, etc. I reiterate, within the context described above, including the effects of multiple impacts of end-stage AD on the brain, how can it (the brain) even be able to temporarily mount a very-very fast broad-span adaptation and almost full reboot of itself, do so with severely damaged hardware and software, and then go completely off-line before dying? You believe that current knowledge explains terminal lucidity and I do not. To me, something is amiss. However, that we have divergent views on this matter is a suitable “état de fait”. Finally, I will be taking a respite from posting as I have other duties to attend.

I may have been a bit wordy in explaining my position.  To simplify, lucid behavioral expression is largely dependent on the connection and exchanges between the neocortex and the thalamus.  Between these two components the thalamus is more vital to our survival and brain function than the neocortex.  The thalamus importance is suggested by how little cortical structure is required for behavioral expression and how nothing happens in the brain without thalamic function.  Lucidity can occur with a severely degrade cortex because it is not as essential to that state as the thalamus' ability to rewire and adapt its function to limited cortical function.

Behavioral efference (output) is coordinated through thalamic function; therefore, lucid behaviors are an output of thalamic function.  To attenuate, refine, and focus its behavioral output, the thalamus relies on a healthy cortex throughout the life of a healthy individual.  When there's degradation in the brain, this doesn't necessarily infer degradation of thalamic function. When we see moments of lucidity in AD patients this suggests that their thalamus has adapted new cortical connection to express that lucidity.  Those connections may become tenuous as the AD cortex continues to degrade.  Sporadic periods of lucidity suggest the tenuous nature of the neural connectivity between the cortex and thalamus in a deteriorating neural environment--like a damaged wire connecting a lamp to its power source.    

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On 12/28/2023 at 8:54 PM, DrmDoc said:

To simplify, lucid behavioral expression is largely dependent on the connection and exchanges between the neocortex and the thalamus. 

AD dysregulates the connection and exchanges between the neocortex and the thalamus

"We present here several lines of evidence that suggest that dysregulation of the corticothalamic network may be a common denominator that contributes to the diverse cognitive and behavioral alterations in AD."

" However, alterations in the corticothalamic network are most likely responsible for a number of other deficits that accompany AD such as sleep fragmentation, attention deficits, cognitive processing deficits, and non-convulsive seizures. Notably, many of these other symptoms become evident even prior to memory deficits."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5854522/

On 12/28/2023 at 8:54 PM, DrmDoc said:

 Lucidity can occur with a severely degrade cortex because it is not as essential to that state as the thalamus' ability to rewire and adapt its function to limited cortical function.

 

AD degrades the thalamus’ ability to rewire and adapt its function to limited cortical function

"Impaired functional connextivity of the thalamus in Alzheimer's disease and mild cognitive impairement: a resting-state fMRI study"

https://pubmed.ncbi.nlm.nih.gov/23905993/

Our DTI analyses indicate that the integrity of thalamic connectivity is progressively disrupted following cognitive decline in AD and that DTI parameters in the column and body of the fornix show promise as potential markers for the early diagnosis of AD and for monitoring disease progression.

https://pubmed.ncbi.nlm.nih.gov/26141074/

On 12/28/2023 at 8:54 PM, DrmDoc said:

 When there's degradation in the brain, this doesn't necessarily infer degradation of thalamic function. 

AD and dementia degrades thalamic function

"Thalamus pathology is an important contributor to cognitive and functional decline, and it might be argued that the thalamus has been somewhat overlooked as an important player in dementia. In this review, we provide a comprehensive overview of thalamus anatomy and function, with an emphasis on human cognition and behavior, and discuss emerging insights on the role of thalamus pathology in dementia."

When the central integrator disintegrates: A review of the role of the thalamus in cognition and dementia - Biesbroek - Alzheimer's & Dementia - Wiley Online Library

"Increasing evidence points to the thalamus as an important hub in the clinical symptomatology of the disease, with the ‘limbic thalamus’ been described as especially vulnerable."

"The results showed widespread thalamic nuclei atrophy in EOAD and LOAD compared to their respective healthy control groups, with EOAD showing additional atrophy in the centromedian and ventral lateral posterior nuclei compared to YHC."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10313877/

 

On 12/28/2023 at 8:54 PM, DrmDoc said:

When we see moments of lucidity in AD patients this suggests that their thalamus has adapted new cortical connection to express that lucidity.   

I have not found any evidence corroborating this suggestion. It may be a valid hypothesis, but remains unsubstantiated.

On 12/28/2023 at 8:54 PM, DrmDoc said:

Those connections may become tenuous as the AD cortex continues to degrade.  Sporadic periods of lucidity suggest the tenuous nature of the neural connectivity between the cortex and thalamus in a deteriorating neural environment--like a damaged wire connecting a lamp to its power source.    

I have not found either any evidence on these statements either. 

On 12/28/2023 at 8:54 PM, DrmDoc said:

I may have been a bit wordy in explaining my position.  To simplify, lucid behavioral expression is largely dependent on the connection and exchanges between the neocortex and the thalamus.  Between these two components the thalamus is more vital to our survival and brain function than the neocortex.  The thalamus importance is suggested by how little cortical structure is required for behavioral expression and how nothing happens in the brain without thalamic function.  Lucidity can occur with a severely degrade cortex because it is not as essential to that state as the thalamus' ability to rewire and adapt its function to limited cortical function.

Behavioral efference (output) is coordinated through thalamic function; therefore, lucid behaviors are an output of thalamic function.  To attenuate, refine, and focus its behavioral output, the thalamus relies on a healthy cortex throughout the life of a healthy individual.  When there's degradation in the brain, this doesn't necessarily infer degradation of thalamic function. When we see moments of lucidity in AD patients this suggests that their thalamus has adapted new cortical connection to express that lucidity.  Those connections may become tenuous as the AD cortex continues to degrade.  Sporadic periods of lucidity suggest the tenuous nature of the neural connectivity between the cortex and thalamus in a deteriorating neural environment--like a damaged wire connecting a lamp to its power source.    

The following link summarizes many of the diverse effects of alzheimer on the thalamus, its function and connectivity to other brain areas.

Here is one excerpt of The effect of alzheimer's disease of the thalamus

"The thalamus is one of the earliest brain regions to be affected by amyloid deposition in AD (Ryan et al., 2013). Our review shows that AD impacts both the thalamus itself (e.g., decrease in volume and cell loss), as well as thalamus’s connections to other brain regions, including hippocampus, Papez circuit, the retrosplenial cortex, and other cortical areas."

https://www.researchgate.net/profile/Rasu-Karki/publication/354341403_The_effect_of_Alzheimer's_disease_on_the_thalamus/links/6419001b92cfd54f84186534/The-effect-of-Alzheimers-disease-on-the-thalamus.pdf

I reiterate, within a severe disease context, how can the brain even be able to temporarily mount a very fast broad-span adaptation and almost full reboot of itself, do so with severely damaged hardware and software, and then go completely off-line before dying? You believe that current knowledge explains terminal lucidity and I do not. To me, something is amiss.

Respectfully! 

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2 hours ago, Luc Turpin said:

AD dysregulates the connection and exchanges between the neocortex and the thalamus

"We present here several lines of evidence that suggest that dysregulation of the corticothalamic network may be a common denominator that contributes to the diverse cognitive and behavioral alterations in AD."

" However, alterations in the corticothalamic network are most likely responsible for a number of other deficits that accompany AD such as sleep fragmentation, attention deficits, cognitive processing deficits, and non-convulsive seizures. Notably, many of these other symptoms become evident even prior to memory deficits."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5854522/

AD degrades the thalamus’ ability to rewire and adapt its function to limited cortical function

"Impaired functional connextivity of the thalamus in Alzheimer's disease and mild cognitive impairement: a resting-state fMRI study"

https://pubmed.ncbi.nlm.nih.gov/23905993/

Our DTI analyses indicate that the integrity of thalamic connectivity is progressively disrupted following cognitive decline in AD and that DTI parameters in the column and body of the fornix show promise as potential markers for the early diagnosis of AD and for monitoring disease progression.

https://pubmed.ncbi.nlm.nih.gov/26141074/

AD and dementia degrades thalamic function

"Thalamus pathology is an important contributor to cognitive and functional decline, and it might be argued that the thalamus has been somewhat overlooked as an important player in dementia. In this review, we provide a comprehensive overview of thalamus anatomy and function, with an emphasis on human cognition and behavior, and discuss emerging insights on the role of thalamus pathology in dementia."

When the central integrator disintegrates: A review of the role of the thalamus in cognition and dementia - Biesbroek - Alzheimer's & Dementia - Wiley Online Library

"Increasing evidence points to the thalamus as an important hub in the clinical symptomatology of the disease, with the ‘limbic thalamus’ been described as especially vulnerable."

"The results showed widespread thalamic nuclei atrophy in EOAD and LOAD compared to their respective healthy control groups, with EOAD showing additional atrophy in the centromedian and ventral lateral posterior nuclei compared to YHC."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10313877/

 

I have not found any evidence corroborating this suggestion. It may be a valid hypothesis, but remains unsubstantiated.

I have not found either any evidence on these statements either. 

The following link summarizes many of the diverse effects of alzheimer on the thalamus, its function and connectivity to other brain areas.

Here is one excerpt of The effect of alzheimer's disease of the thalamus

"The thalamus is one of the earliest brain regions to be affected by amyloid deposition in AD (Ryan et al., 2013). Our review shows that AD impacts both the thalamus itself (e.g., decrease in volume and cell loss), as well as thalamus’s connections to other brain regions, including hippocampus, Papez circuit, the retrosplenial cortex, and other cortical areas."

https://www.researchgate.net/profile/Rasu-Karki/publication/354341403_The_effect_of_Alzheimer's_disease_on_the_thalamus/links/6419001b92cfd54f84186534/The-effect-of-Alzheimers-disease-on-the-thalamus.pdf

I reiterate, within a severe disease context, how can the brain even be able to temporarily mount a very fast broad-span adaptation and almost full reboot of itself, do so with severely damaged hardware and software, and then go completely off-line before dying? You believe that current knowledge explains terminal lucidity and I do not. To me, something is amiss.

Respectfully! 

Citations aside for the moment, consider the objective evidence which is that no expression of lucidity exists without some connection between the cortex and thalamus. Consider the distinction between a mildly impaired and severely impaired thalamus in that mild impairment is likely not sufficient to obstruct periods of lucidity.  None of the citations you've provided suggested impairments that would prevent occassional expression of lucid behaviors with sufficient function and connectivity with the brain--succinctly, there's no behavioral expressions without sufficient brain function and connectivity.

Although AD progression can severely damage the connectivity between the thalamus and cortex, periods of lucidity can persist with sufficient function and connection between the thalamus and cortex. This sufficient function and connection is proved by your observance of lucidity expression within a severely compromised AD neural environment.  The observance that lucidity can persist with a severely damaged brain isn't evidence of anything particularly miraculous, it is merely a testament to the plasticity of our central nervous system amid periods of severe distress.

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1 hour ago, DrmDoc said:

Citations aside for the moment, consider the objective evidence which is that no expression of lucidity exists without some connection between the cortex and thalamus. Consider the distinction between a mildly impaired and severely impaired thalamus in that mild impairment is likely not sufficient to obstruct periods of lucidity.  None of the citations you've provided suggested impairments that would prevent occassional expression of lucid behaviors with sufficient function and connectivity with the brain--succinctly, there's no behavioral expressions without sufficient brain function and connectivity.

Although AD progression can severely damage the connectivity between the thalamus and cortex, periods of lucidity can persist with sufficient function and connection between the thalamus and cortex. This sufficient function and connection is proved by your observance of lucidity expression within a severely compromised AD neural environment.  The observance that lucidity can persist with a severely damaged brain isn't evidence of anything particularly miraculous, it is merely a testament to the plasticity of our central nervous system amid periods of severe distress.

I think that your last post speaks to the crux of the matter. I agree that there should not be any behavioral expressions without sufficient brain function and connectivity. But the data may be (not definitive, but may be) telling us that at a critical junction (between life and death), something else or something more is at play. Let's make the following postulates for end-stage AD: cortico-thalamic link sufficiently maintained; thalamus sufficiently functional; brain still benefiting from plasticity and still seeking homeostasis. Why then do we not see progressively diminishing periods of behavioral expressions followed by progressively increasing periods of non-behavioral expression? Not linear, but average regression! What we usually see in late-stage AD is a long period (months, year) of almost complete non-behavioral expression (typical of significant brain degradation) followed by a brief (hours, day), robust (near full functional) and very-late (close to death (hours, days)) spontaneous burst of behavioral expression. Near death appears to be, but not always, a determining factor here. I am sure that you can find counter points to my points. But isn’t it strange that these things called terminal (hours) or paradoxical (days) lucidity happen mostly near death, when the body is maximally degraded by AD! Also, I am not looking for a miracle to explain what is going on, but a mechanism.  Maybe electro-magnetic wave bursts; very speculative. Maybe sheer willingness to survive; also, very speculative. Finaly, I do not think that we can settle this matter as we would need data that is currently unavailable to do so.

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2 hours ago, Luc Turpin said:

I think that your last post speaks to the crux of the matter. I agree that there should not be any behavioral expressions without sufficient brain function and connectivity. But the data may be (not definitive, but may be) telling us that at a critical junction (between life and death), something else or something more is at play. Let's make the following postulates for end-stage AD: cortico-thalamic link sufficiently maintained; thalamus sufficiently functional; brain still benefiting from plasticity and still seeking homeostasis. Why then do we not see progressively diminishing periods of behavioral expressions followed by progressively increasing periods of non-behavioral expression? Not linear, but average regression! What we usually see in late-stage AD is a long period (months, year) of almost complete non-behavioral expression (typical of significant brain degradation) followed by a brief (hours, day), robust (near full functional) and very-late (close to death (hours, days)) spontaneous burst of behavioral expression. Near death appears to be, but not always, a determining factor here. I am sure that you can find counter points to my points. But isn’t it strange that these things called terminal (hours) or paradoxical (days) lucidity happen mostly near death, when the body is maximally degraded by AD! Also, I am not looking for a miracle to explain what is going on, but a mechanism.  Maybe electro-magnetic wave bursts; very speculative. Maybe sheer willingness to survive; also, very speculative. Finaly, I do not think that we can settle this matter as we would need data that is currently unavailable to do so.

A burst of energetic behavioral expressions near death after a pregressively degenerative brain condition isn't miraculous especially if the neural apparatus for such expression remains sufficiently functional--which it must be for such expressions to occur.  What's left is for us to investigate what neural apparatus remains in place that has allowed for near normal behavior expression amid a severely degradated brain state. 

The observation that these burst of enegetic expressions occurs near death suggest a power-up in a system where the power supplied by limited resources have been redirected from less functional pathways to those that remain sufficiently functional to produce those expressions.  Again, this isn't particularly miraculous given what we aready understand about the nature of plasticity in brain function. 

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14 hours ago, DrmDoc said:

A burst of energetic behavioral expressions near death after a pregressively degenerative brain condition isn't miraculous especially if the neural apparatus for such expression remains sufficiently functional--which it must be for such expressions to occur.  

  Again, this isn't particularly miraculous given what we aready understand about the nature of plasticity in brain function. 

I am not looking for a miracle, but a more satisfactory understanding of terminal lucidity and possible ramifications in the on-going debate on mind-brain connection.

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2 minutes ago, Luc Turpin said:

I am not looking for a miracle, but a more satisfactory understanding of terminal lucidity and possible ramifications in the on-going debate on mind-brain connection.

Yes, but it appears only extraordinary findings will satisfy your quest for understanding rather than findings that are clearly ordinary. The ordinary answer to your inquiry resides in the resiliency of our physiology, which itself is truly extraordinary--imho.

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1 hour ago, DrmDoc said:

Yes, but it appears only extraordinary findings will satisfy your quest for understanding rather than findings that are clearly ordinary. The ordinary answer to your inquiry resides in the resiliency of our physiology, which itself is truly extraordinary--imho.

We both agree to disagree on terminal lucidity and both agree on the extraordinary nature of our physiology.

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  • 5 months later...

Why I find that there is something wrong with our understanding of the mind-brain connection!

Part I

After decades of scientific investigation and ongoing debate, no center has yet been found in the brain for subjective experience. Where the “I” resides in the machine remains elusive.

Here is a summary by Jon Lieff based on years of peering through scientific papers:

“Current science has no explanation for subjective experience”.

“Recent findings show that for most mental events, almost the entire brain is part of wide circuits signaling in milliseconds. No modules have been found, including modules for awareness. In fact, integration of all regions seems to be more relevant than modules. As someone slips into coma and anesthesia, modules appear when people are definitely unconscious. When aware, more widespread integration appears”.

“There has been no evidence of a center of the brain. Previous theories of what brain regions are necessary for consciousness did not pan out. An old disproven theory includes the frontal parietal region. Theories of gamma rays correlating with awareness are outmoded. But, the search continues in study of circuits, regions and brain waves. Perhaps brain waves in smaller regions may be relevant. One way to start researching is to find minimum regions or circuits of brain that allow perception of any type or action that appears to have a purpose”.

“There are many brain regions that don’t directly contribute to experience of specific content. Damage to the large cerebellum doesn’t affect perception experiences much, if at all”.

“Brainstem damage is devastating to all experience. It appears that brainstem and hypothalamus are background regions necessary for subjective experience, but not involved in awareness, the content or experience. Event subcortical regions that modulate content are not really necessary in sleep”.

“Many regions determine emotional states, but aren’t the experience of an emotion. Basal ganglia damage decreases motivation and emotion. But even with extensive damage and some cognitive deficits, patients can be aware with subjective experience”.

 

“Another region under the insula cortex has been studied for its relation to subjective experience. Several case reports of damage to this area have conflicting results and one had awareness and subjective experience”.

 

“Thalamus integrates sensory data. Studies show lesions cause decreased motor ability and poor communication. They can cause coma or not and they have conflicting results about awareness. There doesn’t seem to be a direct correlation with the content of awareness”.

 

“Studies of cortex regions are complex. Primary visual regions appear to be related to identification of visual stimuli, not its content. Higher regions co relate to the content not the stimulus”.

 

“Studies show inconsistent results in the primary visual region (V1). Lesions in V1 produce unconscious awareness of vision called blindsight. They perform as if they see it but don’t have the experience of seeing it. Other lesions show that V1 is not sufficient for conscious perception of sights. Other primary sensory regions for touch and hearing have not had extensive research”.

 

“Another theory is that frontal cortex is related to conscious perception and dorsal unconscious and with movements. But, research shows that both are necessary for visual subjective awareness. Findings about the frontal parietal cortex are inconsistent. Consciousness doesn’t need a frontal lobe. Even lobectomies don’t stop subjective experience. Other lesions in the frontal region leave subjective experience, while affecting particular cognitive abilities”.

 

“Studies of loss of consciousness find the posterior medial cortex most correlated with awareness”.

 

“Studies of posterior cortex of several types relate it to subjective experience of content. Some provide stimuli and see relations of expectations and performance. Sleep studies also point to this region. During dreaming, frontal activity is low compared to awake states. fMRI studies show activity in these regions that correlate with visual stimuli as well. Electrical stimulation of brain regions also shows triggering of specific experiences with posterior cortex. These include faces and wanting to move”.

 

“Neuronal responses of scenes and people rapidly travel through many brain regions (in 100 milliseconds). This includes multiple parts of the cortex visual systems. It also includes more top down neurons related to perception. These complex feedback circuits appear to be necessary for subjective experience”.

 

“There have been suggestions that particular large neurons (von Economo neurons) in cortex layer 5 are related to subjective experience. These neurons are also called spindle neurons. But, recent studies show that these may be more related to unconscious behavior. Thin tufted pyramidal cells in layer 5A and 6 are connected heavily to many cortical regions. Even more connected are supra granular pyramidal neurons, with many feedback connections. These neurons also have a unique spontaneous activity (called neuronal avalanches) that could relate to integration of experience content. In animals, this region is correlated with sensory awareness”.

 

“For some time, gamma waves in visual cortex have been thought to be related to subjective awareness in vision. Waves were thought to bind details to an experience with synchronous oscillations in the gamma range. More recent studies show high frequency gamma waves more related to attention and middle range to whether the stimulus is seen or not. Gamma waves occur in NREM sleep, anesthesia, seizures and unconscious experience. This new data shows gamma waves are not necessary for visual experience and are not correlated with awareness”.

 

“Evoked potentials are another way to study brain responses. Another possible marker of consciousness was thought to be a particular evoked potential. P3b occurs 300 milliseconds after a stimulus of sight or hearing. More recent data show some subjective content do not trigger it and sometimes it is triggered without content. Conscious patients with damaged brains don’t have it. 40% of coma patients have it. Findings are not at all consistent. Recently, another evoked potential has emerged as possibly related. This is 100 milliseconds after a stimulus and is in the same posterior cortex region as the other possible candidates. Another finding on EEG is also being studied. This is called activated or desynchronized EEG and occurs during attention. It consists of low voltage fast activity and deep sleep’s high voltage slow activity. Loss of consciousness occurs at the same time as thalamic switching from tonic to bursts of firing. Slow waves are related to cortex switching on and off up and down states. Those subcortical brain regions changes occur with decrease of activating systems. High amplitude slow waves are related to loss of consciousness. Changes in the waves occur in transition from coma to barely conscious and then awake causing delta to theta to alpha. But, it is not clear this reflects awareness. Slow waves can occur in conscious people in epilepsy. Previous studies have tried to correlate whole brain recordings to consciousness. But, local patterns may be more relevant. Sleep cortex can be activated while whole brain EEGs have only slow waves. Local activation in the parietal occipital region is related to visual dreams and then awakening. Recent EEG studies show that there are many possible local events in conscious people. There are fewer variations when unconscious. Also consciousness might involve more integrated states rather than different modules with various activities.

 

“Most current approaches to finding places in the brain related to consciousness or awareness do not corroborate old theories of networks in the frontal parietal regions. Recent research is focused on activity in a much more narrow region near the overlap of the temporal-parietal-occipital regions. Some of these appear to be triggered by content of awareness—such as faces. The older larger circuits appear related to attention focused on particular areas, not simple awareness. In fact, most regions of the brain have something to do with awareness and consciousness, but this doesn’t qualify them as a location of consciousness”.

“There is still no understanding of how subjective experience binds together all that is part of our daily experience of awareness. Most events in the brain involve large brain wide circuits traversed in milliseconds. A recent study implied meaning of words is not in a language center, but distributed throughout the entire brain. The same is true for memory, which appears to be very distributed. Some pre frontal regions are related to experiences of various types. Default mode circuits appear to be related to day dreaming and identity, not simple awareness. Other similar frontal regions have nothing directly to do with consciousness. With so much top-down effects in perception, it is not clear how much sensory regions contribute to simple awareness. Brainstem reticular formation and parts of the thalamus help create the necessary activation of circuits for awareness but are not awareness per se.No brain region simply reflects consciousness. Some regions are correlated with content of awareness. For now, this search will continue with no definition of consciousness or subjective experience. We are left with our every day experience”.

 

Cerebral cortex & Deep Grey Matter

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3115284/#:~:text='%20The%20mind%20cannot%20be%20localised,grey%20matter%20form%20important%20components.

 

Motor cortex - somato-cognitive action network,

https://www.reuters.com/lifestyle/science/scientists-identify-mind-body-nexus-human-brain-2023-04-19/

 

White Matter

https://medicalxpress.com/news/2023-10-scientists-powerful-brain-white.html

 

Right and left parietal junction; posterior cingulate

https://journals.sagepub.com/doi/abs/10.1111/j.1467-9280.2006.01768.x

 

Cortical midline, mirror neuron system

https://www.sciencedirect.com/science/article/pii/S1878929314000048

 

Dorsomedial subsystem (at least for part of it)

https://academic.oup.com/scan/article/15/1/63/5733878

 

Medial prefrontal cortex, posterior cingulate, bilateral temporoparietal junction, posterior superior temporal sulcus

 

https://books.google.ca/books?hl=en&lr=&id=tCgTDgAAQBAJ&oi=fnd&pg=PA83&dq=location+of+mind+in+brain&ots=QvqpCYGDjs&sig=XVLpTURu2jikwB9Gs5HIN9au9ys#v=onepage&q=location%20of%20mind%20in%20brain&f=false

 

Anatomical regions far apart from one another

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6871093/

 

Its in multiple areas of the brain

https://link.springer.com/chapter/10.1007/978-94-011-4996-9_26

 

Specialized and domain general structure working in tandem

https://researchoutreach.org/articles/explaining-mind-works-new-theory/

 

No brain boundaries between thinking, feeling, deciding, etc.

https://www.quantamagazine.org/mental-phenomena-dont-map-into-the-brain-as-expected-20210824/

 

Its not even in the brain

https://qz.com/866352/scientists-say-your-mind-isnt-confined-to-your-brain-or-even-your-body

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1 hour ago, Luc Turpin said:

After decades of scientific investigation and ongoing debate, no center has yet been found in the brain for subjective experience. Where the “I” resides in the machine remains elusive.

Why do you assume one exists?

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36 minutes ago, swansont said:

Why do you assume one exists?

I am not assuming this, but the neuroscience community has been trying for decades to locate it because it would greatly bolster the mind from brain hypothesis. On the contrary, I am assuming that there is none, which may be more in line with the mind through brain hypothesis whereby the brain is a transducer, not a creator of mind.

I will be posting other parts of my argumentation militating for a different perspective of mind, and then, maybe, I will be on firmer ground to discuss matters further.

Note: my purpose in all of this is to demonstrate that there are major flaws with our understanding of the mind-brain connection and that one possible avenue of reconciliation with data is mind through brain. I will also try and demonstrate that mind is not only confined to higher primates.

 

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28 minutes ago, Luc Turpin said:

I am not assuming this, but the neuroscience community has been trying for decades to locate it because it would greatly bolster the mind from brain hypothesis. On the contrary, I am assuming that there is none, which may be more in line with the mind through brain hypothesis whereby the brain is a transducer, not a creator of mind.

“Is there a center of the mind” is a question for science to investigate.

Assuming an answer, one way or another, is not; it lends itself to cherry-picking results to support the assumption. (cherry-picking is bad)

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11 minutes ago, swansont said:

“Is there a center of the mind” is a question for science to investigate.

Assuming an answer, one way or another, is not; it lends itself to cherry-picking results to support the assumption. (cherry-picking is bad)

1- agree

2- agree, but there was  bias towards finding it, and this perspective comes from reading many neuroscience discussion-position papers. However, there was no cherry picking as it was not found and the search continues without abandonment.

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9 minutes ago, Luc Turpin said:

The bias debate is unimportant here; what is important is that there appears to be no center for subjective experience.

Because information is collected across multiple streams and sources, each with different weighting and timing. 

Your question is a bit like asking what is the center of the atmosphere or the center of the ocean or the center of space. 

Even if there was a clear simple answer that would satisfy your ape brain, the answer itself would change from one moment to the next since the system is ever evolving and never static. 

Subjective experience is deeply tied to focus and attention. Where is your focus when taking a math test, or where is it when running a sprint? Where is it when you’re doing either of those things without having had good in the past week or without having slept in the last several days?

The problem is you trying to force a single monolithic oversimplified answer to a complex system level question. 

Edited by iNow
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1 hour ago, iNow said:

Because information is collected across multiple streams and sources, each with different weighting and timing. 

Your question is a bit like asking what is the center of the atmosphere or the center of the ocean or the center of space. 

Even if there was a clear simple answer that would satisfy your ape brain, the answer itself would change from one moment to the next since the system is ever evolving and never static. 

Subjective experience is deeply tied to focus and attention. Where is your focus when taking a math test, or where is it when running a sprint? Where is it when you’re doing either of those things without having had good in the past week or without having slept in the last several days?

The problem is you trying to force a single monolithic oversimplified answer to a complex system level question. 

The question being asked does not come from me, but from the neuroscience field. The field has been trying to answer this question for decades by probing the brain with no clear answer as demonstrated in the Lieff post above. If someone is forcing a single monolithic oversimplified answer to a complex system level question it is not I, as I agree with you that there is no simple answer to this one..

 

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Why I find that there is something wrong with our understanding of the mind-brain connection!

Part II

There is no understanding on how the mind works through the brain (the hard-problem). There are many theories about it, but no consensus in sight for the near future.

From Theories of consciousness by Anil K. Seth and Tim Bayne

Recent years have seen a blossoming of theories about the biological and physical basis of consciousness”.

“To clarify this complicated landscape, we review four prominent theoretical approaches to consciousness: higher-order theories, global workspace theories, re-entry and predictive processing theories and integrated information theory”.

https://www.nature.com/articles/s41583-022-00587-4

 

From Consciousness: Theories and Models by B. Boars and A.K. Seth

“What should we expect from a neural theory of consciousness? One thing we should not ask for is that the theory produce consciousness. After all, a theory of hurricanes is not itself windy. Rather, a useful theory should help move from establishing correlations between brain activity and conscious experience toward developing explanations that link features of brain activity with features of conscious phenomenology, as well as accounting for the relevant experimental evidence. Because consciousness is a rich biological phenomenon, the theories surveyed in this article vary in emphasis, level of abstraction, and the extent to which they provide satisfying explanations of conscious phenomena. At present, no single effort accounts for all the evidence, but we have seen marked progress in the last few decades.”

https://www.sciencedirect.com/topics/psychology/theory-of-consciousness#:~:text=Following%20is%20a%20brief%20review,integrated%20information%20theory%20(IIT).

 

From Cognitive theories of consciousness by V. de Gardelle and S. Kouider

“In the present article, we first overview the precursors that allowed the development of cognitive theories of consciousness, and in particular we consider the notions of attention, working-memory, modularity, and the distinction between automatic and controlled processes. Then we present a selection of influential contemporary accounts of consciousness on the basis of three themes: consciousness results from specific architectural elements within the cognitive system (the theories by Baars, Prinz, Tononi); some features of consciousness are in fact illusory (the theories by Dennett and Wegner); and consciousness is about learning (the theories by O’Regan and Noë, Cleeremans, Lau). We conclude this article by considering that these cognitive theories have to set a bridge between the philosophical hard problem of consciousness and neurobiological approaches.”

https://www.sciencedirect.com/science/article/abs/pii/B9780123738738000773

 

From Reward and punishments, goal-directed behavior and consciousness by Newton Ressler, in Neuroscience & Biobehavioral Reviews

theory of consciousness based upon an organism's interactions with environmental stimuli has been developed by Damasio [4]. In this theory, interconnected brain stem nuclei and somatosensory cortices, which monitor and control the body state, give rise to a sense of self. A collection of protoself systems has its states mapped in a correlated way with the mappings of sensory objects. Consciousness reflects a neurodynamic melding of object mappings and self-mappings. This melding involves changes in the protoself systems (generated by engagement with the object) that enhances the object and brings it into consciousness. Consciousness thus stems from the feelings that are associated with the formation of re-representations of the organism interacting with the world. It is thus a higher order system involving neural patterns that re-represent first order occurrences. The present model provides an alternate possibility to Damasio's theory, in which the assumptions of a higher order system are not required”.

 

From Artificial Intelligence and Consciousness by D. Gamez, O. Holand, in Reference Module in Neuroscience and Biobehavioral Psychology

“Many people have conjectured that consciousness might be linked to cognitive characteristics, such as emotions, imagination and a model of the self. If consciousness depends on functions at the cognitive level, then it should be possible to realize it on any piece of hardware that is capable of carrying out the appropriate processing. One example of a cognitive theory of consciousness is the axiomatic theory of Igor Aleksander, which claims that imagination, emotion, depiction, volition and attention are minimally necessary for consciousness, and any natural or artificial system that implements these axioms is judged to be conscious according to this theory. Global workspace theory is another cognitive architecture that can be implemented on many different types of hardware, and Thomas Metzinger's phenomenal self model and constraints on conscious experience are also largely independent of the physical system.”

 

From Folk Theories of Consciousness by B.F. Malle in Encyclopedia of Consciousness

 

“People’s folk theory of consciousness encompasses three prototypes of conscious mental functioning: monitoring (awareness), choice, and subjective experience. All three are embedded in a broader folk theory of mind and thus closely linked to the concept of intentionality, action explanation, and a conception of free will. At least some of the prototypes of consciousness play a critical role in the assignment of personhood and responsibility. Recent discussions question the viability of folk conceptions of consciousness in light of work on the unconscious and neuroscience. Thus far this work appears to complement folk conceptions without contradicting them.”

 

From Artificial Intelligence and Consciousness by O. Holland, D. Gamez in Encyclopedia of Consciousness

“Many other theories of consciousness have positive implications for the possibility of creating consciousness in artificial systems. To begin with, the pantheist claim that all matter is conscious to some degree suggests that computers and robots are conscious even when they are switched off. David Rosenthal's claim that consciousness depends on a higher-order thought about another mental state is not linked to any particular implementation, and a number of connections have been made between consciousness and virtual machines that can run on any type of hardware. Some researchers have claimed that inner speech helps to constitute our sense of self and agency and may be important to consciousness as well. If this is the case, it might be possible to use the work on language acquisition in AI to develop conscious systems.”

 

From Neural signs and mechanisms of consciousness: Is there a potential convergence of theories of consciousness in sight? By Georg Northoff, Victor Lamme in Neuroscience & Biobehavioral Reviews

“Various theories for the neural basis of consciousness have been proposed, suggesting a diversity of neural signs and mechanisms. We ask to what extent this diversity is real, or whether many theories share the same basic ideas with a potential for convergence towards a more unified theory of the neural basis of consciousness. For that purpose, we review and compare the various neural signs, measures, and mechanisms proposed in the different theories. We demonstrate that different theories focus on neural signs and measures of distinct aspects of neural activity including stimulus-related, prestimulus, and resting state activity as well as on distinct features of consciousness. Therefore, the various mechanisms proposed in the different theories may, in part, complement each other. Together, we provide insight into the shared basis and convergences (and, in part, discrepancies) of the different theories of consciousness. We conclude that the different theories concern distinct aspects of both neural activity and consciousness which, as we suppose, may be integrated and nested within the brain’s overall temporo-spatial dynamics”.

 

From Hard Criteria for empirical theories of consciousness By Adrien Doerig, Aaron Schurger and Michael H. Herzog

“Consciousness is now a well-established field of empirical research. A large body of experimental results has been accumulated and is steadily growing. In parallel, many Theories of Consciousness (ToCs) have been proposed. These theories are diverse in nature, ranging from computational to neurophysiological and quantum theoretical approaches. This contrasts with other fields of natural science, which host a smaller number of competing theories. We suggest that one reason for this abundance of extremely different theories may be the lack of stringent criteria specifying how empirical data constrains ToCs. First, we argue that consciousness is a well-defined topic from an empirical point of view and motivate a purely empirical stance on the quest for consciousness. Second, we present a checklist of criteria that, we propose, empirical ToCs need to cope with. Third, we review 13 of the most influential ToCs and subject them to the criteria. Our analysis helps to situate these different ToCs in the theoretical landscapeand sheds light on their strengths and weaknesses from a strictly empirical point of view.”

https://www.tandfonline.com/doi/full/10.1080/17588928.2020.1772214

From Comparing theories of consciousness: why it matters and how to do it by Simon Hviid Del Pin, Zuzanna Skóra, Kristian Sandberg, Morten Overgaard, Michał Wierzchoń 

The theoretical landscape of scientific studies of consciousness has flourished. Today, even multiple versions of the same theory are sometimes available. To advance the field, these theories should be directly compared to determine which are better at predicting and explaining empirical data. Systematic inquiries of this sort are seen in many subfields in cognitive psychology and neuroscience, e.g. in working memory. Nonetheless, when we surveyed publications on consciousness research, we found that most focused on a single theory. When ‘comparisons’ happened, they were often verbal and non-systematic. This fact in itself could be a contributing reason for the lack of convergence between theories in consciousness research. In this paper, we focus on how to compare theories of consciousness to ensure that the comparisons are meaningful, e.g. whether their predictions are parallel or contrasting. We evaluate how theories are typically compared in consciousness research and related subdisciplines in cognitive psychology and neuroscience, and we provide an example of our approach. We then examine the different reasons why direct comparisons between theories are rarely seen. One possible explanation is the unique nature of the consciousness phenomenon. We conclude that the field should embrace this uniqueness, and we set out the features that a theory of consciousness should account for.

 

https://academic.oup.com/nc/article/2021/2/niab019/6354404?login=false

 

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Why I find that there is something wrong with our understanding of the mind-brain connection!

Part III

The brain is much-much more complex than anticipated. Here are only three in a vast array of brain processes that demonstrate this complexity. How much more complexity will be required before we establish that more than randomness and mechanistic processes are at play here?

Note: Apologies for the length of the post as it was necessary to show complexity.

_________________________________________________________________________________________________________

1-     How Human Brains are built by Jon Lieff

“The development of the human brain involves orchestration of thousands of different kinds of cells in an array of trillions. A vast range of molecular and cellular processes operate in brain development over a very long period of time. “

“The human brain starts as a tube and then becomes fantastically organized. It produces special regions of increased stem cell activity, with many more diverse stem cells than other species. “

“Adults have approximately 86 billion neurons including the brain and spinal cord. There are another 100 billion glial cells. The cortex has 16 billion neurons and 160 trillion synapses. In the entire brain there are hundreds of trillions of synapses. It is very hard to believe, but it has been calculated there are 100,000 miles of myelinated axons in each brain.”

“In the fetus, 3.8 million new neurons are minted each hour for the cortex and 4.6 million for the entire brain. In late fetal life, 42 million synapses are formed each minute in the cortex. How can so many cells be produced, specified and placed in circuits?”

“In order for the three-dimensional structure of the cortex to be formed, cells need to be able to be in their proper coordinates—radial direction and tangent plane. This information is somehow expressed in genetic networks through transcription factors. Cells, also, respond to signals from axons from the thalamus. This very detailed layered structure is maintained because of different types of neurons in specific placements, which are defined by connections to incoming and outgoing axon connections.”

“There are 46 human chromosomes with a total of around 6 DNA billion base pairs (letters in the DNA code). The word “gene” has changed its meaning recently and is considered by some to include DNA that produces proteins (from RNA) as well as DNA that produces RNA that has functional effects without making proteins. Approximately 20,000 protein genes exist with another 40,000 genes that make only RNA but not protein (non coding RNA or ncRNA). Much of this non-coding RNA regulates the genetic activity in making RNAs and proteins. Recent research has found 400,000 particles that enhance DNA production and 70,000 promoters that trigger DNA production. Each type of cell (each type of neuron) has different promoters, enhancers and other RNAs.”

“Most of the recently found non coding RNAs are used to build the brain. Almost all of the genes (90%) are used differently in each brain region and at each different stage.” 

“Some genetic networks only operate at particular periods of time in all regions. Some large networks work for long periods, mainly in infancy, childhood and adolescence.” 

“The gene networks operate in clusters that start up in many places at once and coordinate the complex changes that are occurring in structure and function”. 

“The triggering of the gene clusters at exactly timed sequences and in the exact locations are part of the vast regulation of genes. It involves many players. Once clusters are triggered however, the strength of that production is regulated by a variety of molecules that increase production of a particular molecule (enhancers and promoters), that stop the production (silencers) and that alter the relationship of promoters and enhancers (insulators)”.

“These regulatory molecules themselves have places for multiple other molecules to bind.” 

“But, along with these, the epigenetic tags have very complex and important interactions as well. There are now more than forty different kinds of tags that are placed on DNA and histones that affect these processes. The most well known are methyl and acetyl groups in various specific stops in DNA and histone, but there are many others.”

“The epigenetic tags combine with all the other factors including non coding RNAs and the 3D alterations of chromatin that affect the production of particular clusters of genes. Recent research shows that these epigenetic tags can all respond to stimulation from outside as well (the well known idea of experience modeling brain structures). For example the addition of a methyl group to the cysteine code of DNA seems to be a critical stimulus of cortex development.”

“To make things even more complex, jumping genes have also been implicated as part of this regulation, particular for the human brain. These mobile DNA particles function at times as regulating and transcription factors for other DNA.”

________________________________________________________________________________________________________________

2-     From Jumping Gene regulation by Jon Lieff

“The regulation of DNA is fantastically complex with many different layers: changing 3D shapes of the chromatin and loops of DNA; regional differences in nuclear DNA; large numbers of different epigenetic tags on DNA nucleotides and protective protein histone molecules; complex DNA repair mechanisms and alternative messenger RNA splicing; hundreds of thousands of transcription factors; and many different kinds of small and large RNAs that influence every aspect of the process.”

“Another critical factor of genetic regulation has been recently discovered. Jumping genes make up 50% of all human DNA and the battle between the effects of jumping genes and the cell’s attempts to stop their influence is one of the major drivers of all evolution. Although many different important physiological effects have been found directly related to jumping genes and viruses, new research now shows that jumping genes directly regulate many vital aspects of brain processes.

“Most are not aware that fifty percent of the DNA in each human cell is in the form of mobile jumping genes—strands of DNA called transposable elements (TE) that have the ability to sew themselves in and out of DNA as well as move to different sections and to place copies in different sections. The mobile strands of DNA in the jumping gene can create new types of proteins, disrupt the entire genetic process and provide new sources of regulation of DNA through many kinds of RNA effects. The jumping gene can provide new epigenetic changes, as well. Previous posts noted that these jumping genes and alternative messenger RNA splicing are especially critical for the human brain and its evolution.”

“It is not really possible to distinguish material inserted from viruses, virus-like particles and jumping genes except by their specific content traced to a virus. 8% of human DNA is from retroviruses and has been vital to human evolution”. 

“An epigenetic immune system in the nucleus battles the jumping genes for control of the cell and control of evolution. “

“The two opposing forces of mobile elements and epigenetics are very related—the proliferation of mobile DNA particles and the cell’s epigenetic mechanisms to control them. With environmental stress, the genome responds with activation of epigenetic processes. This increases the capacity to withstand this stress using new mechanisms, which can be inherited through epigenetic mechanisms. When the stress subsides, then the increased amount of jumping genes activity also subsides. Recently, more has been discovered about the cell’s response to stress and the regulation by jumping genes that is described in this post”.

“LINEs are several thousand base pair strands produced from DNA into a messenger RNA that produces several critical protein enzymes. These include a protein that binds to the RNA and another than makes a copy of the DNA and inserts it back into the genome. This is done by making two nicks at particular places in the DNA. SINEs, which are 85 to 500 base pairs, don’t make any proteins and instead use those made by LINEs.”

“The placement of LINEs and SINEs are not random. SINEs are in regions where the DNA is most often used to make proteins. LINEs are mostly in other areas. Such a large piece of DNA in a LINE would certainly disrupt any gene. SINEs mix in better with the functioning genes and often develop regulatory functions. Having so many SINEs and LINEs in human cells provide regions of new activity and new problems.”

“Another surprising recent finding is that proteins provided by LINEs are not just used by SINEs and LINEs, but, also, help other ordinary messenger RNAs to be copied and inserted.” 

“Cellular stress can come from poisoning or infection with viruses. The cell responds to stress by using jumping genes to regulate the number of active ribosomes that make proteins. Regulating ribosomes is a significant way to defend against viruses that take over the cell’s ribosomes to replicate. It is, also, a way to save valuable ribosomes during a crisis until they are needed again”.

“When stress occurs, the cell needs to take some of the signals out of commission to prevent triggering cell death and to only use what is necessary during the crisis. It makes “stress granules” to hide this material from general use. These granules gather up other proteins that would be used to produce new proteins. All of this material waits in the granule until the cellular crisis is over so they can be used again normally. When a poison is given, such as arsenic, particular jumping genes form complexes that bind sequestered material into the stress granules. When stress is over, the cell produces more RNAs that are used by the jumping genes and then the sequestered material is released”.

“This process, also, stops ribosomes from making virus proteins as part of the innate immune system fighting viruses. This is an example of jumping genes helping the cell to fight off random viruses by regulating the use of ribosomes.”

“The cell generally tries to not allow the function of the RNAs made from SINEs in human organs. But, SINEs respond to stress signals (such as heat shock) and this triggers the SINEs to make a very large amount of RNAs. During this stress many genes are triggered, while ordinary genes are inhibited. In this way the SINEs become an important part of the stress response.”

“Jumping genes have many other complicated genetic effects. SINEs can affect the critical splicing of messenger RNA. One particularly important and very common family of SINEs in humans are called Alu elements. There are many types of Alu elements, which are made of about three hundred base pairs. This strand of DNA was originally named from a bacteria Arthrobacter luteus, which produces an enzyme that cuts DNA in particular places. Alu has been implicated in cancer and other diseases.”

“Alu elements have many different effects because of their ability to splice the new jumping genes in many different places. At first they reside in introns (the parts of the RNA that are cut out during messenger RNA splicing). But, they can easily become part of the exon (the part that is used for the protein) and become part of the messenger RNA that will make a protein. A previous post noted that alternative mRNA splicing is most often used in the human brain and is critical for the development of its unique capabilities. Five percent of all alternative splicing in human cells are from Alu sequences. Whenever an Alu piece gets into an exon, it becomes part of the alternative splices. Therefore, it is critical in the development of the unique characteristics of the human brain. A large percentage of the new brain alternative splices (that is, unique proteins) include Alu exons. Somehow, proteins that bind to the RNAs involved with the editing of messenger can associate with the SINE signals and the complex splicing machines.”

“Another trick from the Alu is based on the similarity between different Alu versions. Two Alu transcripts can be oriented in different directions and can help form circular non-coding RNAs. Circular RNAs are just now being discovered and many unique properties including regulation of genes. Circular RNA is found in unique regions of the brain and other tissues and in unique stages of development.

"A particular sequence of codes is called “polyadenylation” or poly(A) that consists of multiple adenine bases in a row. This poly (A) normally forms a tail at the end of messenger RNAs, which helps as a signal in the normal process of making a protein from the messenger RNA. Also, many of the very long non-coding RNAs that have dramatic effects on the 3D shape of large sections of chromosomes have this sequence at the end called 3’. There are particular code sequences that help create these tails and poly (A) sections in the RNA; these code sequences are called a polyadenylation signal or PASLINEs and SINEs are filled with adenine and often produce more of the PAS signals. In particular Alu can create these PAS, alterations in gene functioning are unique in the human species and the human brain."

"The actions of RNAs were described in a previous post (Intelligent Small and Large RNAs) as acting either nearby (cis) or far away and globally (trans). Alu elements in particular have great influence on whether a messenger RNA will be effective based on competition with other elements in the process. Other complex factors are microRNAs made from LINEs and SINEs, which promote more microRNA and which bind as promoters on the messenger RNA. These Alu elements are in 6% of all human messenger RNAs. By using complex mechanisms involving long non-coding RNAsAlu elements can cause the decay of important messenger RNA mechanisms and influence which proteins are made. In particular, these are influential in neuronal migration.”

“RNAs are formed in the nucleus from the DNA and then transported outside of the nucleus through the nuclear pores to the vicinity of ribosomes usually in the endoplasmic reticulum to make proteins. However, the unique effects of these SINEs, LINES, microRNAs and Alu elements create a unique compartment called “paraspeckles” that are still in the nucleus. This small compartment near the edge of the nucleus works in conjunction with multiple proteins for RNA functions and long non-coding RNAs. They produce unusual proteins that stay in the nucleus and can influence DNA regulation. Some other Alu elements trigger the proteins to be transported out of the nucleus. Extremely complex processes related to paraspeckles have just been discovered and are not yet fully understood. But, they have definite effects in regulation of DNA.”

“The response to stress of Alu elements occurs in the cytoplasm, not the nucleus. Stress granules usually are in the endoplasmic reticulum of the cytoplasm. (Stress granules can sometimes appear in the nucleus.) These are large aggregations of proteins and RNA that are produced when the cell is under stress. It includes many messenger RNAs that did not complete the job of making a protein. The Alu elements attach to enzymes and repress their activity. This can influence a large amount of proteins. They can act nearby or in distant regions where proteins are made. This process is made much more complex during cell replication when there is a breakdown of the separation of nucleus and cytoplasm when the nuclear envelop breaks down. The jumping genes have significant roles in the mitotic process.”

“Another process increases the use of messenger RNA through long-range mechanisms. Stress, including virus infection and heat shock, increases the amount of Alu RNAs. This, also, occurs when the production of proteins is decreased. This occurs in different ways when other animals are stressed. While the stress is occurring, the Alu stops local factors that inhibit production, thereby increasing production of specific local proteins.”

“One way cells fight RNA viruses is to alter their RNA by editing adenosine to inosine in the molecule. The inosine is read by the process as a guanosine and therefore the production of sensible proteins is disrupted. Most of these occur in Alu elements.”

“While some effects of LINEs and SINEs are positive for cell regulation, many are not and cause disease. Alu elements are the most common insertions in the germ line of humans and in particular make promoters there. Almost a hundred different genetic diseases have been identified from these insertions. Many others occur in the organs, rather than sperms and eggs. Cancers in particular use techniques to remove methylation tags on the LINE and SINE promoters. But, these occur also in brain diseases, including Rhett syndrome and schizophrenia.”

“One of the major defenses against jumping genes is methylation tags. Recent research finds even more methylation on histones protecting SINEs. Other defense mechanisms include ways to eliminate particular messenger RNAs produced by the jumping genes. Two particular types of small RNAs are active against LINE and SINE RNAs. These are endogenous small interfering RNAs or endo-siRNAs and PIWI-interacting RNAS or piRNAs. (See post on the many kinds of RNAs in the Brain.) There are specific enzyme complexes that cut specific messenger RNA with Alu elements and other jumping genes. Also, autophagy mechanisms gather mobile element RNAs in their lysosomes vesicles.”

“Recent dramatic findings show that jumping genes are very active in the brain. These SINEs and LINEs are actively altering and regulating neurons and other cells. Some of the changes have been incorporated into day-to-day functions. There is strong evidence that these jumping genes and their effects on alternative functions have been significant in the development of the human brain. This goes along with the evidence that the human brain uses the most alternative messenger RNA splicing. While these findings are still too complex to fully understand, it does appear to be part of the picture that has developed where jumping genes and cellular defense against them are crucial for evolution in general and especially so for the evolution of the human brain.”

_____________________________________________________________________________

3-     From the Enormous Complexity of Transport Along the Axon by Jon LIeff

“Some scientists consider scaffolding fibers and tubules in the neuron to be the seat of consciousness. They respond instantly to any mental event with massive movement and construction—building and rebuilding the structures for dendrite spines and axon boutons at synapses in the ever-changing neuron.”

“Microtubules are the critical highways for materials, mitochondria and vesicles along the vast length of the axon. Many neuro-degenerative diseases can be traced to dysfunction of microtubules. In fact, the cause of Alzheimer’s might be the disintegration of tau molecules that provide strength and stability to the microtubule structures.”

 “Scientists are amazed that microscopic materials can be transported more than several feet along one neuron that goes from the spinal cord to the foot. This is equivalent scale to a person carrying a package walking along the wall of China.

Now, research is showing many different elaborate motors and hundreds of adaptors and factors utilized in this transport. In fact, the extremely complex mechanisms are different for each type of cargo—messenger RNA, small molecules, vesicles filled with neurotrophins, mitochondria, ribosomes, and huge organelles like lysosomes and phagosomes. Each cargo is tagged for its destination. Also, each section of the axon—the initial segment and regions far from the cell body—have different types of transport regulation. Research is showing the enormous complexity of transport along the axon.”

“While there are three basic types of scaffolding tubules—actin, intermediate filaments, and the larger microtubules—it is the microtubules that provide transport along the axon. “

“The microtubule is built as a spiral cylinder with a positive charge on the growing leading edge and a minus charge on the other. Transport away from the cell body carries lipids, proteins, energy producing mitochondria, vesicles of all types and other materials for the synapse. Transport back to the cell body is critical for mitochondria going back and forth, removal of debris in vesicles and signals related to damage of the distant axon regions. In fact, defects in the ability to transport debris might be the primary cause of Alzheimer’s disorder.”

“Microtubules make a reliable shape for a track where motors shuffle or step along carrying many kinds of loads. There are many motors that use these tracks. But, the two major ones in the neuron are the protein motor kinesin, which moves away from the cell center toward the synapse and the protein motor dynein, which moves material toward the cell center. Rapid growth of axons occurs with many parallel microtubules enlarging at the plus end. The organization of microtubules is much more variable and complex in the smaller, but equally rapidly growing dendrites. For the dendrite, the minus end near the cell body is either connected to the centrosome (an organelle that serves as the main microtubule organizing center) or they are capped for stability.”

“There are a host of associated proteins that maintain stability. A famous one is tau that holds these arrays of microtubules together until they collapse in Alzheimer’s and form neurofibrillary tangle. There are, however, many other proteins associated with microtubules that, when defective, produce disease. These include many different scaffolding proteins, motors and adaptors used to transport different material. These associated proteins can, even, regulate the specific motors on the microtubule.”

“Kinesins are the motors that travel from the cell body to the synapse. Dyneins go back to the cell body. They were both discovered thirty years ago and operate with a stepping motion as if they are walking carrying a bundle.”

“Kinesin-1 takes proteins, organelles, RNA and vesicles at a rate of around 1um/second (a micrometer is 0.000001 of a meter). The structure includes two heavy subunits and two light subunits. The light chains are involved in mechanisms for stopping the transport. They move toward the plus growing end of the microtubule. Each step is 8 nm long (a nanometer is 0.000000001 of a meter). This step has a strong attachment and force and can win a match with an opposing motor. But, they still can detach when it is too difficult. New proteins are transported very rapidly. Organelles have been clocked with movement of 400 mm/day (which is 1um/second).” 

“The moving part of Kinesin-2 is either a single molecule or made of multiple subunits. It specializes in carrying material for membranes. The attachment is not as strong as K1 and can detach if presented with a tug or war from an opposing motor."

"Kinesin-3 is altered based on what it is carrying and can be made to travel much faster when carrying critical organelles. K3 carry sacs with neurotransmitters and materials for the synapse. These can operate with increased force because of the importance of their cargo that can overcome opposing transport and obstacles”.

“Unlike kinesin, the active dynein motor subunit is made from one gene. The intermediate and light chains have two genes each. It, also, has heavy and light chains for different structures used in carrying different loads. These subunits can self assemble into different arrangements for different situations.”

“Dynein travels very fast, but can, also, take back and side steps, unlike kinesins. It is not as strong as kinesin and loses direct battles with it when traveling in opposite directions along the same microtubule. But, its sideways movement makes it very effective in overcoming obstacles. Dynein can work in teams of motors for larger more complex cargo.”

“Dynein, most of the time, needs a factor called dynactin, a very complex molecule made of several proteins that activates dynein for use. It is critical for the function of neurons by binding to the microtubule and the dynein motor. Dynactin has many different binding sites and has a wide range of activity including special functions in the initial axon region and other distant regions.” 

"Many cargoes use multiple motors at once, sometimes as many as a dozen. Heavy or large cargoes, such as lysosomes, have many attached motors for transport that work together. These teams of motors can consist of kinesin-1, kinesin-2, and dynein together. Kinesin 1 and 2 work together to transport vesicles with prions inside. Autophagosomes (for cleaning debris) travel a long way on the axon with dynein and kinesin working together."

"How are all these different motors regulated? Is each regulated or is there overall direction; or are the motors competing? One model says kinesin is strongly regulated and less for dynein. However, very new research finds that in many cases, the scaffolding molecules regulate this tug of war. (Another finding that supports consciousness in these molecules)."

"Each type of cargo, motor and adaptor seems to be regulated differently."

"Kinesein-1 has been shown, at times, to regulate itself and change its speed and force."

"There are, in fact, many factors that alter movement in different ways with different cargoes. Dynein regulation can be caused by attachment and detachment of ATP energy molecules, which alters its force. This causes the motor to attach more strongly to the microtubule with less movement. Another factor, the protein huntingtin, regulates vesicles with BDNF and autophagosomes, and is relevant to Huntington’s disease. There are many enzymes involved in this process."

"Each large organelle takes part in the regulation of its own movement and they use quite different mechanisms. For some organelles, specific motors stay with an organelle even if the motor is not being used at that time. Specific groups of opposing motors move very large organelles. These mechanisms are very complex and include kinase enzymes, multiple molecular cascades, attaching phosphorus energy particles, and scaffolding protein activity."

"Neuropeptidesneurotransmitters, and neurotrophins are critical to neuron function and are carried in special vesicles called dense core or granular vesicles by kinesin-3. The mechanism for granular vesicles changes the structure of the kinesin-3 subunits as well as the specific adaptors. These particular vesicles cannot be returned and new ones must be sent all the way from the cell body to the synapses. Each is tagged for delivery to specific dendrites and axon tips with different material. There are specific regulators of the movement as it approaches the target. The dynein is disabled at the site to avoid return of useless sacs. The sacs are recycled locally."

"Protein that is the precursor of amyloid, APP (amyloid precursor protein), is carried in a vesicle at very rapid rates mostly away from the cell body. The mechanism includes a particular molecule that is phosphorylated to provide the switch determining direction."

"BDNF (brain derived neurotropic factoris a critical molecule for neuronal function and is transported from the cell body to the synapse. The vesicle transport, uniquely, uses huntingtin and makes a scaffolding structure with kinesin-1 and dynein motors. Huntingtin phosphorylation is the switch to go forward and the opposite dephorphorylation goes backward. (A defective huntingtin causes Hungtington’s disease)".

"Neurotrophins are factors that are secreted locally near the synapse and maintain the health and very life of the neuron. Without them the neuron will die. These critical molecules bind at the presynaptic terminal–the end of the axon. From there, they are transported backwards to the cell body where they stimulate networks of genes to maintain the health of the neuron. It is a signal from the tissue where the axon has landed to help keep the neuron alive."

"Neurotrophins are taken into the cell in vesicles (signaling endosomes) and taken along the microtubules to the cell body. This transport is very active, fueled by ATP production along the axon from mitochondria. Mitochondria are moved along the microtubules to provide this needed energy (30% of mitochondria are moving at any one time)."

"The movement of mitochondria has unique regulation. Mitochondria are slowed near the synapse so they will stay there and provide energy. The signal to slow is the increased levels of calcium from the neuron’s action potential at very particular places near the synapse."

"Those mitochondria that are nearby–15nm away–are not affected. But, if they travel through the area of increased calcium they stop. When specific dendrites are very active, the mitochondria maintain a higher level of energy production. There are many complex mechanisms of the transport motors and adaptors to provide this calcium effect."

"Microbes’ decision-making ability, communication, and group behavior were discussed. It described the process of mitochondrial fission and fusion that is highly regulated through the endoplasmic reticulum of the neuron. Mitochondria within the neuron function as a microbe community working together for the goal of providing energy throughout the very complex neuron. They communicate with each with various signals and to the cell through intermittent contact with the endoplasmic reticulum."

"Critical vesicles, such as endosomesphagosomes and lysosomes, are carried on the transport systems, many going back and forth rapidly. Like mitochondria these are essential organelles that are needed to clean up debris or bring information to different regions. There are unique mechanisms for the transport away from the cell body using adaptors that link to the subunits of kinesin-1 and 2, and others to dynein."

"The transport of hundreds of different structural materials to constantly build and rebuild the structure of the axon is slower than that of the organelles. There are two different slow speeds for these materials—1 mm per day and 10 mm per day. The slower speed is for intermediate filaments and tubulin (to make microtubules). The faster rate is for a large number of smaller molecules. It is much harder for scientists to study the slow transport because of the need for very long observation of living microscopic material."

"Different intermediate filament assembled units are transported by kineisin-1 and dynein. One of the subunits binds directly to the motors. The transport seems to be in small movements with rests in between. The transport of actin and microtubule structures is not as well known. It is especially difficult to study microtubules, because they are built up and broken down so rapidly. Tubulin for microtubules is transported either as two molecules or as small microtubule assemblies."

"More than two hundred other molecules are transported to be used in construction. Synapsin is one critical protein that combines into complexes, which latch onto passing motors. The slow rate of transport is related to the complex attaching and reattaching with periods of travel and waiting. Despite this type of stop and go system, the slow transport provides three times the material as the fast transit. The proteins that travel from the spinal cord to the foot can take from four months to a year for transport. " 

"Each region of the axon has very different scaffolding structures and different mechanisms. "

"In the initial segment there is a very specific structure with unique stabilizing molecules. This region makes sure that cargoes headed for the dendrites and the cell body don’t start travelling down the long axon. Some cargoes are targeted for the dendrite, but start down the axon and are stopped and re routed. Unique adaptors and modifiers for microtubules in this region help this process."

"The distant regions of the axons direct the return of cargoes all along the axon to the cell body by unique mechanisms. The growth of microtubules in these distant regions is different. It is much more active and variable with many different plus ends appearing. There are special proteins in this region that interact with the active plus ends. Dynactin, also, interacts with the special proteins at the plus ends. These complex very active mechanisms appear to give direction to transport heading back to the cell body."

"Since the electrical charge seems to be related to this increased intelligent activity of the microtubules, it is has be questioned whether electrical fields are involved. Please see the post on electrical fields and gradients determining cellular behavior."

"While many of the proteins are manufactured in the cell body and transported the long way to the synapse, there is increasing evidence that there is, also, local ribosome activity all along the axon and in the dendrites. Large ribosomes are, first, transported to distant sites. To use the local ribosomes, messenger RNA is transported to these regions."

"Research has uncovered more about the production of local proteins in the dendrite. In order to transport messenger RNA they need to be altered. The usual mechanisms to find a ribosome are held in check until they travel to the distant ribosome. Specially altered messenger RNAs are put in a granule vesicle with the necessary proteins and even some large ribosomes. These specially packed vesicles go back and forth in both directions—wherever needed—and seem at times to oscillate."

"The movement of messenger RNA vesicles is greatly increased when there is nerve injury, as well as by some chemical signals. When there is injury, special proteins are manufactured that bind to the motors stimulating more rapid transport of supplies. There are, also, genetic activating factors that stimulate more protein manufacturing. With nerve injury, complex multi protein structures produce transport back to the cell. They signal the activation of genetic machinery to rev up manufacturing for repair. This process involves many steps from a variety of enzymes triggered by energy rich phosphorus."

"A faster signal of the injury is increased calcium at the injury site that radiates back to the cell body. This process affects the histone regulating enzymes in the nucleus causing more genetic activity to make needed materials for transport. Chemical signals can, also, increase transport of more messenger RNA vesicles. Special factors, like NGF, can signal production of proteins from messenger RNAs in distant sites."

"Surprisingly, even before injury, vesicles filled with messenger RNA are placed along the axon, ready to be used when needed."

"The transport motors stepping along the axon use ATP as their energy source. Kinesin-1 uses one ATP for every step of 8 nm. Each large vesicle or organelle has multiple motors walking. If there are conflicts and tug of wars, the amount of energy is increased. A typical transit can use millions of energy molecules. Dynein’s steps are much larger, up to 32nm, but it can go backwards and sideways as well as forward. Dynein uses many motors per vesicle—up to a dozen. This process, also uses a million energy molecules."

"Given the large amount of energy required for axon transport, it is not surprising that a second mechanism has been discovered unique to transport. While mitochondria probably supply most of the energy, it appears that vesicles have glycolytic enzymes that produce energy particles linked to the vesicles as they travel on the microtubules."

"In fact, the energy needs of neuronal baseline activity are very high and transport by motors is not a great percentage of the total. The brain, weighing three pounds, uses at least 20% of all the energy of the body. Much of the usage is the constant electrical activity along the axons, which requires maintenance of a large number of membrane channels. The vesicle energy backup system could work in the regions between mitochondria. This type of energy can only be used for the larger cargoes with vesicles."

"Another important factor is the energy support from glia cells. Glia provide materials for glycolysis as well."

"A mental event triggers instantaneous building and tearing down of scaffolding molecules. The scaffolding molecules are critical for every function of the neuron, including rapid changes of neuroplasticity. Somehow, they are the circuit boards and Lego blocks of information flow in the neuron. It is hard to imagine how this direction can occur or where it is coming from."

"Because of this, some scientists suspect there might be quantum computer activity in the middle of the microtubule. This information at the quantum scale would communicate with other tubules and direct the microtubules and other molecules. Such a scenario, also, fits a theory of mind interacting with quantum states."

"In any case, something must direct these massively complex, shifting structures. Does a neuron think with its microtubules? How does this process connect with human thinking?"

"The transport microtubule system is extremely complicated, where very specific multiple motors, factors and adaptors operate together to transport many different kinds of cargoes. The complexity of the transport system includes tagging and choosing each molecule for specific cargos and specific destinations, while choosing multiple unique co factors and adaptors. Totally different assemblies are chosen for building materials, neurotrophins, mitochondria, and large vesicles like lysosomes. Each uses multiple motors at a time. It is difficult to imagine the direction for all these processes."

"With all of this complex activity and regulation responding instantly to thought and the alterations of neuroplasticity, how can anyone think that this process is in any way random?"

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Can you imagine having a conversation with some folks and suddenly someone jumps up on the coffee table and spews out a rant like that? That's not discussion, that's a lecture nobody signed up for.

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