The Mutation You Want: It Protects the Brain, Extends Life
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
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A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
In a mouse model of frontotemporal dementia, a trifecta of tau mutations hobbles newborn neurons in the dentate gyrus.
Organoids patterned on the dorsal human forebrain consistently contain a set of cells native to the cerebral cortex, and develop along the same trajectory as fetal brains. Could they become the standard for organoid research?
A compound that only blocks presenilin 1-containing secretases beat back leukemia in mice—without side effects caused by broad-spectrum inhibitors.
Serum from young mice boosted synapses and activity in human neurons. Researchers credit the proteins SPARCL1 and THBS4.
Researchers identify a specific SCF ligase that clears fibrillar but not physiologic forms of α-synuclein, suggesting potential for a targeted therapeutic approach.
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.
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?
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.
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.
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.
In healthy, older adults specific EEG patterns correlated with plaque and tangle burdens.
New strains have amyloid, neurodegeneration, and neuroinflammation, all against a background of natural genetic variation.
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
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