HArticle out today
Drugs that quell brain inflammation reverse dementia
https://news.berkeley.edu/2019/12/04/drugs-th...-dementia/
After age 70, nearly 60% of adults have leaky blood- brain barriers, according to Friedman’s magnetic resonance imaging (MRI) studies.
But reading other studies what is causing these T Cells to cross over and attack? I think they are being called to brain through their ccr5 receptor, which is partly why maraviroc is working with stroke victims, stopping the crossing to the bbb to begin with.
Example:
https://www.jimmunol.org/content/jimmunol/182...8.full.pdf
Our results suggest that intracerebral A-Betta interaction with RAGE at BBB up-regulates endothelial CCR5 expression and causes circulating T cell infiltration in the brain in AD.
Also
https://www.cell.com/cell/pdf/S0092-8674(19)30107-2.pdf
CCR5 is differentially upregulated in neurons after stroke
Knockdown of CCR5 induces motor recovery after stroke and improves cognition after TBI Treatment with an FDA-approved drug, maraviroc induces recovery after stroke and TBI
Human carriers for CCR5delta32 have better outcomes after stroke
Also explanation in addition to T cells,
https://www.sciencemag.org/news/2019/02/hiv-d...ter-stroke
Blocking CCR5 seemed to help maintain connections between neurons adjacent to the injured site. And it caused neurons in motor regions to sprout more projections to the opposite side of the brain, a process that might help a mouse relearn lost movements.
What CCR5 does in the poststroke brain is hazy. Surging CCR5 is part of the inflammatory response to stroke, says Robyn Klein, a neuroimmunologist at Washington University School of Medicine in St. Louis, Missouri. In flammatory molecules may prompt neurons to express more of this chemokine receptor. In the developing brain, chemokines are known to influence how neurons migrate and connect. After stroke, they seem to decrease the number of connection sites on neurons near the damage. (How that process hinders regrowth and recovery isn't clear.)
Carmichael notes that blocking CCR5 also caused neurons to express genes that increase their excitability, making them fire more readily. He suspects that neurons boost CCR5 after a stroke to dampen their activity and lie low to avoid a deadly cellular frenzy known as excitotoxicity. But because the protein then sticks around, that protective mechanism gets in the way of recovery
Drugs that quell brain inflammation reverse dementia
https://news.berkeley.edu/2019/12/04/drugs-th...-dementia/
After age 70, nearly 60% of adults have leaky blood- brain barriers, according to Friedman’s magnetic resonance imaging (MRI) studies.
But reading other studies what is causing these T Cells to cross over and attack? I think they are being called to brain through their ccr5 receptor, which is partly why maraviroc is working with stroke victims, stopping the crossing to the bbb to begin with.
Example:
https://www.jimmunol.org/content/jimmunol/182...8.full.pdf
Our results suggest that intracerebral A-Betta interaction with RAGE at BBB up-regulates endothelial CCR5 expression and causes circulating T cell infiltration in the brain in AD.
Also
https://www.cell.com/cell/pdf/S0092-8674(19)30107-2.pdf
CCR5 is differentially upregulated in neurons after stroke
Knockdown of CCR5 induces motor recovery after stroke and improves cognition after TBI Treatment with an FDA-approved drug, maraviroc induces recovery after stroke and TBI
Human carriers for CCR5delta32 have better outcomes after stroke
Also explanation in addition to T cells,
https://www.sciencemag.org/news/2019/02/hiv-d...ter-stroke
Blocking CCR5 seemed to help maintain connections between neurons adjacent to the injured site. And it caused neurons in motor regions to sprout more projections to the opposite side of the brain, a process that might help a mouse relearn lost movements.
What CCR5 does in the poststroke brain is hazy. Surging CCR5 is part of the inflammatory response to stroke, says Robyn Klein, a neuroimmunologist at Washington University School of Medicine in St. Louis, Missouri. In flammatory molecules may prompt neurons to express more of this chemokine receptor. In the developing brain, chemokines are known to influence how neurons migrate and connect. After stroke, they seem to decrease the number of connection sites on neurons near the damage. (How that process hinders regrowth and recovery isn't clear.)
Carmichael notes that blocking CCR5 also caused neurons to express genes that increase their excitability, making them fire more readily. He suspects that neurons boost CCR5 after a stroke to dampen their activity and lie low to avoid a deadly cellular frenzy known as excitotoxicity. But because the protein then sticks around, that protective mechanism gets in the way of recovery
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