Alzheimer’s Risk Variants Found in Diverse Populations
A large meta-analysis turns up 16 new loci.
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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.
Triggered by senescent cells, macrophages spew a protease that dissolves junctions between the cells that separate CSF from blood.
In a mouse model of amyloidosis, the BACE1 enzyme snipped subunits of the GABA(A) receptor, squelching its inhibitory function.
Thinning out glycoproteins in the brain blood vessels of young mice allowed blood to leak into the brain. Promoting glycosylation in old mice strengthened the barrier.
In neurons, FAM171A2 opens the door to toxic fibrils. An approved cancer drug slams it shut.
The man has lots of plaques but few tangles 18 years after his expected age of onset; potential protective factors include extensive heat shock protein expression.
In neurons from a person with HD, knocking down MSH3 kept CAG nucleotide expansions from growing even longer.
The marker detected plaques and tangles with 90 percent accuracy in almost 200 autopsy-confirmed frontotemporal dementia cases.
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