Using single-nuclei or cell sorting, three separate research groups sequenced RNA from human postmortem brains. They unveiled AD-associated gene-expression signatures, but disease-related transcriptomes from human microglia were quite different from those in mice.
Using an array of receptors to sense neurons in peril, microglia make matters worse by taking bites out of the struggling cells.
At Quebec conference, human herpesvirus experts devoted a day to consider whether their favorite villain might play a hand in Alzheimer’s pathogenesis.
In a new, inducible mouse model, poly(GR) damages mitochondria, but its effect is reversible. In flies, turning off transcription of hexanucleotide expansion protects cells.
Research on postmortem human brain strengthens the idea that an ebbing of neurogenesis may underlie cognitive decline.
Phase 1b data show that Biogen’s BIIB092 lowers N-terminal tau fragments in cerebrospinal fluid by more than 90 percent.
In a mouse model of frontotemporal dementia, a trifecta of tau mutations hobbles newborn neurons in the dentate gyrus.
A compound that only blocks presenilin 1-containing secretases beat back leukemia in mice—without side effects caused by broad-spectrum inhibitors.
In Taiwan, interferon treatment for chronic hepatitis C infection appears to have reduced the incidence of Parkinson’s disease.
Using different techniques, contestants vied for the best way to tell which ADNI participants would develop clinical, cognitive, or imaging signs of Alzheimer’s disease.
Two groups create mice for imaging and manipulation of microglia, leaving related cells untouched. The trick? Piggybacking on Tmem119 expression.
One rare variant protects ApoE4 carriers, others put noncarriers at risk.
Today, the creators of bioRχiv launch a repository for preliminary medical research, including clinical trial data.
Microglial responses to Alzheimer’s risk variants, and to tau pathology, appear to show a sex difference. Microglia in male versus female mice use different biological mechanisms to maintain homeostasis.
At a joint Keystone symposia, researchers reported how microglia, via TREM2, compress plaques and rein in the pathogenic distortion of neurites into swollen stubs. Without TREM2, these damaged neuronal processes served as fertile ground for tau propagation.