“The SALIENT-AD trial's focus on neuroinflammation via microglial PET imaging is the closest active clinical readout to this vascular biology because the CCR5-dependent myeloid recruitment mechanism governing plaque vulnerability and neuroinflammatory microglial activation share the same upstream architecture”
Speaking of connecting dots (myocarditis risk with ICI, potential cardioprotective effect of Leronlimab) and extending that implication to AD, the study below just published seems to confirm vascular permeability with consequent recruitment of microglial cells and impedance of amyloid clearance understood through the lens of a copper compound repair mechanism speaks to the importance of disruption of vascular architecture.
https://pubs.acs.org/doi/10.1021/acschemneuro.6c00252
“this study investigated the effect of copper diacetyl bis(4-methyl-3-thiosemicarbazone) (Cu(ATSM)) on brain microvascular abundance and function of P-gp and the associated effects on exogenous Aβ clearance, brain amyloid burden, and cognitive function.”
https://www.monash.edu/pharm/about/news/news-...s-proteins
“Monash University researchers have found in laboratory experiments that a drug which delivers copper to the brain significantly reduces toxic Alzheimer’s proteins and improves long-term spatial memory.
The study, published today in the journal ACS Chemical Neuroscience, shows the compound Cu(ATSM) repairs a vital waste-clearing pump at the blood-brain barrier – unlocking a potential new avenue of therapeutics targeting neurovascular dysfunction, caused by one of the world’s leading causes of death.
Alzheimer’s is driven by the buildup of toxic proteins called amyloid-beta. Normally, the brain flushes these out into the bloodstream through the blood-brain barrier. In Alzheimer’s, the pumps doing the heavy lifting, called P-glycoprotein (P-gp), weaken significantly, clogging the drain and trapping the toxic proteins in the brain.”
https://www.drugtargetreview.com/copper-drug-...15.article
“While the study demonstrated a significant reduction in amyloid-beta levels, researchers are continuing to investigate the precise biological pathways involved in removing the proteins from the brain.
In addition to restoring blood-brain barrier function, the team believes the copper treatment may enhance the activity of microglia, the brain’s immune cells, enabling them to consume and break down toxic plaques more effectively.”
Speaking of connecting dots (myocarditis risk with ICI, potential cardioprotective effect of Leronlimab) and extending that implication to AD, the study below just published seems to confirm vascular permeability with consequent recruitment of microglial cells and impedance of amyloid clearance understood through the lens of a copper compound repair mechanism speaks to the importance of disruption of vascular architecture.
https://pubs.acs.org/doi/10.1021/acschemneuro.6c00252
“this study investigated the effect of copper diacetyl bis(4-methyl-3-thiosemicarbazone) (Cu(ATSM)) on brain microvascular abundance and function of P-gp and the associated effects on exogenous Aβ clearance, brain amyloid burden, and cognitive function.”
https://www.monash.edu/pharm/about/news/news-...s-proteins
“Monash University researchers have found in laboratory experiments that a drug which delivers copper to the brain significantly reduces toxic Alzheimer’s proteins and improves long-term spatial memory.
The study, published today in the journal ACS Chemical Neuroscience, shows the compound Cu(ATSM) repairs a vital waste-clearing pump at the blood-brain barrier – unlocking a potential new avenue of therapeutics targeting neurovascular dysfunction, caused by one of the world’s leading causes of death.
Alzheimer’s is driven by the buildup of toxic proteins called amyloid-beta. Normally, the brain flushes these out into the bloodstream through the blood-brain barrier. In Alzheimer’s, the pumps doing the heavy lifting, called P-glycoprotein (P-gp), weaken significantly, clogging the drain and trapping the toxic proteins in the brain.”
https://www.drugtargetreview.com/copper-drug-...15.article
“While the study demonstrated a significant reduction in amyloid-beta levels, researchers are continuing to investigate the precise biological pathways involved in removing the proteins from the brain.
In addition to restoring blood-brain barrier function, the team believes the copper treatment may enhance the activity of microglia, the brain’s immune cells, enabling them to consume and break down toxic plaques more effectively.”
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