Maybe another mechanism by which Leronlimab can be
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Posted On: 12/25/2024 11:32:50 AM
Maybe another mechanism by which Leronlimab can be a viable treatment for Alzheimer's Disease.
"Dark Microglia and Alzheimer’s Disease: Using electron microscopy, the researchers identified an accumulation of “dark microglia,” a subset of microglia associated with cellular stress and neurodegeneration, in postmortem brain tissues from Alzheimer’s patients. These cells were present at twice the levels seen in healthy-aged individuals.
Toxic Lipid Secretion: The ISR pathway in microglia was shown to drive the synthesis and release of harmful lipids that contribute to synapse loss, a hallmark of Alzheimer’s disease.
Therapeutic Potential: In mouse models, inhibiting ISR activation or lipid synthesis prevented synapse loss and accumulation of neurodegenerative tau proteins, offering a promising pathway for therapeutic intervention.
These findings reveal a critical link between cellular stress and the neurotoxic effects of microglia in Alzheimer’s disease,” said the study’s co-lead author Anna Flury, a member of Ayata’s lab and a Ph.D. student with the CUNY Graduate Center’s Biology Program. “Targeting this pathway may open up new avenues for treatment by either halting the toxic lipid production or preventing the activation of harmful microglial phenotypes.”
Implications for Alzheimer’s Treatment
This research underscores the potential of developing drugs that target specific microglial populations or their stress-induced mechanisms. “Such treatments could significantly slow or even reverse the progression of Alzheimer’s disease, offering hope to millions of patients and their families,” explained co-lead author Leen Aljayousi, a member of Ayata’s lab and a Ph.D. student with the CUNY Graduate Center’s Biology Program."
https://scitechdaily.com/the-hidden-culprit-b...icroscope/
https://www.sciencedirect.com/science/article...4911001110
It looks like the ISR pathway would either be interrupted or regulated by Leronlimab's down regulation of elF2a, and PKR.
Maybe Ohm20 could look this over and verify this statement.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8874...conditions.
This is my opinion only.
Merry Christmas to everyone! GLTUA!
"Dark Microglia and Alzheimer’s Disease: Using electron microscopy, the researchers identified an accumulation of “dark microglia,” a subset of microglia associated with cellular stress and neurodegeneration, in postmortem brain tissues from Alzheimer’s patients. These cells were present at twice the levels seen in healthy-aged individuals.
Toxic Lipid Secretion: The ISR pathway in microglia was shown to drive the synthesis and release of harmful lipids that contribute to synapse loss, a hallmark of Alzheimer’s disease.
Therapeutic Potential: In mouse models, inhibiting ISR activation or lipid synthesis prevented synapse loss and accumulation of neurodegenerative tau proteins, offering a promising pathway for therapeutic intervention.
These findings reveal a critical link between cellular stress and the neurotoxic effects of microglia in Alzheimer’s disease,” said the study’s co-lead author Anna Flury, a member of Ayata’s lab and a Ph.D. student with the CUNY Graduate Center’s Biology Program. “Targeting this pathway may open up new avenues for treatment by either halting the toxic lipid production or preventing the activation of harmful microglial phenotypes.”
Implications for Alzheimer’s Treatment
This research underscores the potential of developing drugs that target specific microglial populations or their stress-induced mechanisms. “Such treatments could significantly slow or even reverse the progression of Alzheimer’s disease, offering hope to millions of patients and their families,” explained co-lead author Leen Aljayousi, a member of Ayata’s lab and a Ph.D. student with the CUNY Graduate Center’s Biology Program."
https://scitechdaily.com/the-hidden-culprit-b...icroscope/
https://www.sciencedirect.com/science/article...4911001110
It looks like the ISR pathway would either be interrupted or regulated by Leronlimab's down regulation of elF2a, and PKR.
Maybe Ohm20 could look this over and verify this statement.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8874...conditions.
This is my opinion only.
Merry Christmas to everyone! GLTUA!
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