Alzheimer’s Risk Variants Found in Diverse Populations
A large meta-analysis turns up 16 new loci.
A large meta-analysis turns up 16 new loci.
Expression of TREM2, ApoE, and complement proteins correlated with extensive plaque clearance in response to Aβ immunotherapy.
Behold the first high-resolution structure of the human Parkinson’s-related kinase bound to mitochondrial membranes.
Meta-analysis of six longitudinal studies finds that, among people who are amyloid-positive, tau PET signal rose faster in women.
Inhibiting this receptor calmed reactive astrocytes and curbed their consumption of synapses in the hippocampus in a mouse amyloidosis model.
The largest single-cell RNA-Seq study of blood cells finds more sex-specific expression changes in PD than AD. The database is accessible online.
In rats, antibodies to the MTBR domain and adjacent C-terminal regions spared synaptic function.
Electronic health records show that various autoimmune disorders put people at higher risk for AD.
As plaques vanish from the brain post-Aβ immunotherapy, what goes on with cells behind the scenes? Using spatial transcriptomics of postmortem brains from people immunized against Aβ 20 years ago, and from one person treated with lecanemab, scientists spotted microglia in the throes of clearing plaques. They pinpointed ApoE, TREM2, complement, and other signals as integral to the response.
In older mice, macrophages in the choroid plexus release a protease that chews up tight junctions between epithelial cells, allowing blood proteins and immune cells to enter the CSF. Senescent cells may spark production of the protease, and blocking it prevented memory loss.
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