Too much or too little serum hemoglobin increases risk for Alzheimer’s and other dementias by 20 percent or more.
As the Alzheimer’s field suffers smackdowns in trials of small molecules and antibodies, antisense oligonucleotides are quietly coming along—and looking safe so far.
A brother’s survival guilt, a journalist tracing her mutation to Lebanon, a student freezing her eggs ahead of a primary prevention trial—DIAN family members are stirring their growing community to act against Alzheimer’s disease.
At AD/PD Conference, New Alzheimer’s Genes Reinforce Known Pathways Expression, Expression, Expression—Time to Get on Board with eQTLs APP Upp: Mutation Nixes Six Amino Acids from Aβ, Spurs Aggregation Parsing How Alzheimer’s Genetic Risk Works Through ...
Nearly 30 years after the first Alzheimer’s gene discoveries, genetics once again drives recruitment, scientific progress, and therapy development in the Dominantly Inherited Alzheimer’s Network.
A tool of modern genetics, expression studies link GWAS hits to specific cell types, providing clues to pathogenesis. Microglia come up again and again.
At AAIC, researchers presented baseline data from an ongoing, five-year study asking whether the anti-Aβ antibody crenezumab can forestall cognitive decline in autosomal-dominant Alzheimer’s disease.
DIAD: Families from Argentina, Canada, Minnesota Rally a Global Community Genetics Propels DIAN Toward Therapies ASOs: Wave of the Future in Alzheimer’s Therapeutics? As DIAN Wraps Up Anti-Aβ Drug Arms, it Sprouts Tau, Primary Prevention Arms On July 13, ...
Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.
Among former National Football League players who died with CTE, tau tangles, crumbling white matter, and arteriolosclerosis independently contributed to dementia.
What’s with all those head-to-head comparison studies of academic and commercial biomarker tests? Could we not just pick one that works, and be done?
In a tauopathy model, knocking out C3 spared synapses and neurons. In an amyloidosis model, deleting C3 preserved dendritic spines, but exacerbated plaque growth.
Older people who lived healthy lifestyles had a third lower risk of dementia than their unhealthy peers, but only if their genetic risk for the disease was low.
Clinical trial design could benefit from new estimates of how slowly amyloid accumulates and how best to detect it at various disease stages.
Loss of ataxin-1 intensifies BACE1 expression, Alzheimer’s pathogenesis. Is that how ataxin GWAS variants increase AD risk?