Unlocking Blood-Brain Barrier Boosts Immunotherapy Efficacy, Lowers ARIA
Roche’s “brain shuttle” antibody, trontinemab, cleared plaque in Phase 1 with little ARIA, highlighting that bypassing vascular amyloid could be the key.
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Roche’s “brain shuttle” antibody, trontinemab, cleared plaque in Phase 1 with little ARIA, highlighting that bypassing vascular amyloid could be the key.
Phase 1b results tease that the small molecule PRI-002 might curb cognitive decline. Phase 2 is slated for early 2024.
In early phase trials, therapy lowering tau translation hinted at cognitive benefit, while going after APP lowered its fragments and Aβ peptides.
At trials conference, multiple amyloid immunotherapy programs reported greatest cognitive benefits for people whose tau tangle deposition has only just begun.
To Recruit for Diverse Alzheimer Trials, Go to the People From St. Louis to Boston, Scientists Grapple with Ethnoracial Divide in AD Biomarkers Treat Before ‘Aβ Bothers Tau,’ Scientists Say at CTAD Moving Forward: RNA-Targeted Attempts at Taking Down Tau,
Across several studies, black/African Americans and Hispanic or Latino people had lower amyloid positivity rates than whites. Scientists are studying why.
Most participants in AD research studies and trials are non-Hispanic whites. At a conference in St. Louis, scientists discussed strategies to include diverse populations.
A new study defined the location and expression profile of this astrocyte subtype, pegging the protein myocilin as a marker.
These imaging abnormalities grew the most in people with many plaques or cerebral amyloid angiopathy pathology, irrespective of cardiovascular risk.
Scientists report that when the TREM2 fragment binds transgelin-2, it weakens phosphorylation of tau in neurons.
At Leiden conference, scientists discussed how shifting cells toward “specialized pro-resolving mediators” could counter inflammation.
The Alzheimer’s risk allele locks microglia in a state of homeostasis. They ignore amyloid plaques and neurofibrillary tangles.
An antibody copying the effects of the protective ApoE variant prevents tau hyperphosphorylation in the mouse eye and brain.
A cholesterol metabolite magnifies pathology in a tauopathy mouse. Microglia need cholesterol to rein in amyloid. ApoE4 jams the fat's export from neuron to glia.
We all know oligodendrocytes maintain myelin. According to scientists at the 2nd Symposium on Lipids in Diseases, they need microglia to do it.
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