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Microglia priming


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Yes, it seems this is a possibility in black are my comments:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5696326/

 Communication between the systemic immune system and the brain and its consequence on microglia is a critical poorly understood component of the inflammatory response to systemic disease (78). Systemic infections activate neural and humoral pathways that communicate with the brain and initiate a coordinated set of metabolic and behavioral changes (79). However, these adaptive responses may become maladaptive when microglia have been “primed” by an ongoing pathology and respond to a systemic inflammatory challenge by switching their phenotype to an aggressive pro-inflammatory state (47), adversely affecting neuronal function and potentially leading to a psychotic decompensation through modulating effects of pro-inflammatory cytokines on neurotransmitter function (47).

https://minerva-access.unimelb.edu.au/handle/11343/234029#:~:text=Accumulating evidence indicates that inflammation,of structural deficits in psychosis.

Peripheral markers of inflammation

As described above microglial activation can have pro- or anti-inflammatory effects. Determining which pathway predominates in psychotic disorders in vivo is currently not possible as the available radioligands do not distinguish between M1 and M2 states.117 Nevertheless, evidence that there may be an imbalance in favor of the M1 pathway comes from studies examining peripheral cytokine levels.118 This suggests that medication-naive first-episode psychosis patients have increased expression of the M1 associated pro-inflammatory cytokines: IL-1B, IL-6 and TNFa.119, 120 Moreover, one of the triggers of M1 activation, S100B, is present at higher levels in individuals with schizophrenia.121 A parallel is seen here with childhood trauma in which raised levels of pro-inflammatory IL-6 and TNF-a,122 and reductions in brain-derived neurotrophic factor expression (a product of the M2 pathway) have been observed.118, 120

But the next paragraph indicates the possibility that inflammation may actually be present before the onset of psychosis, in which case it is still possible that psychosis furthers this inflammatory phenotype, but it does not have to be that way.

There is also evidence that alterations in inflammatory markers may exist well before the onset of psychosis, and may predict progression to psychosis.123 Post-mortem and neuroimaging studies in individuals with schizophrenia provide support for a link between immune activation and damage to both gray and white matter.94, 118, 124, 125, 126 In individuals with schizophrenia, an increase in peripheral cytokines associated with the M1 pathway has been shown to correlate with reductions in both hippocampal,118 and prefrontal cortex volumes.124, 126 A link between cytokine levels and TSPO binding, however, has not been demonstrated,108 which could be because cytokine levels fluctuate.

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