Paper Alert: VCAM1 Opens the Door to Brain Aging
Expression of VCAM1 on the endothelial cells that line the blood-brain barrier allowed aging factors in the plasma to exact their toll on the brain.
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Expression of VCAM1 on the endothelial cells that line the blood-brain barrier allowed aging factors in the plasma to exact their toll on the brain.
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.
Data on ASOs, presented recently at the annual meeting of the American Academy of Neurology, depict RNA-based therapies as broadly on the rise in neurodegenerative diseases.
Antisense Oligonucleotides: Can They Take on ALS, SMA, Prions? Drug Reported to Help Alzheimer’s Patients Sleep Better American Academy of Neurology 2019 Annual Meeting
Research on postmortem human brain strengthens the idea that an ebbing of neurogenesis may underlie cognitive decline.
New potential immunotherapies and insight into single-cell responses were highlights of a small meeting in Denmark.
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.
One rare variant protects ApoE4 carriers, others put noncarriers at risk.
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.
Today, the creators of bioRχiv launch a repository for preliminary medical research, including clinical trial data.
Two groups create mice for imaging and manipulation of microglia, leaving related cells untouched. The trick? Piggybacking on Tmem119 expression.
Through an endocytic process called LANDO, microglia clear β-amyloid and route their used Aβ receptors, including TREM2, back to the plasma membrane. Without it, aggregates pile up outside and form plaques.