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.
Two groups create mice for imaging and manipulation of microglia, leaving related cells untouched. The trick? Piggybacking on Tmem119 expression.
Today, the creators of bioRχiv launch a repository for preliminary medical research, including clinical trial data.
Fully automated immunoassay could offer cost-effective screening for AD.
A meta-analysis of 47 studies suggests CSF NfL is particularly elevated in a select few, suggesting it could help in differential diagnosis.
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
New strains have amyloid, neurodegeneration, and neuroinflammation, all against a background of natural genetic variation.
In healthy, older adults specific EEG patterns correlated with plaque and tangle burdens.
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.
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.
One rare variant protects ApoE4 carriers, others put noncarriers at risk.
In Taiwan, interferon treatment for chronic hepatitis C infection appears to have reduced the incidence of Parkinson’s disease.
In mice, inflammatory microglia must die, and new ones take over for efficient remyelination. Could problems with this changing of the guard contribute to neurological diseases?
Serum from young mice boosted synapses and activity in human neurons. Researchers credit the proteins SPARCL1 and THBS4.
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.