Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.
New genes linked to early and late-onset AD offer up mechanistic insight, potential targets for treatment.
Among former National Football League players who died with CTE, tau tangles, crumbling white matter, and arteriolosclerosis independently contributed to dementia.
Functional variants of AD GWAS hits found in enhancers of myeloid genes.
New evidence suggests the dimers impede clearance of glutamate from synapses, contributing to the hyperexcitability seen early in Alzheimer’s disease.
ApoE2 homozygotes have a dramatically lower risk of AD than even the previously known low-risk E2/3 heterozygotes. More study of this protective allele could reveal roots of resilience.
In 2,144 Colombian ADAD family members, plasma NfL in gene carriers rises as early as two decades before their symptoms start.
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.
Desikan pioneered advances in neuroimaging and neurogenetics, and was known for his passion and collaborative spirit.
The DIAN Trials Unit is nearing the end of its first two secondary prevention trials. It has begun a cognitive run-in period for its next trial, of a tau-based drug, and for a primary prevention study in people as young as 18.
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.
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 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.
Too much or too little serum hemoglobin increases risk for Alzheimer’s and other dementias by 20 percent or more.
RPS25 helps translate repetitive snippets of RNA that are associated with neurodegenerative diseases. Knocking it down reduces protein aggregates and cell death.