TREM2 Mystery: Altered Microglia, No Effect on Plaques
In mouse models, the Alzheimer’s risk gene TREM2 affects microglial behavior but does not lead to more amyloid deposition.
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In mouse models, the Alzheimer’s risk gene TREM2 affects microglial behavior but does not lead to more amyloid deposition.
Scientists report that astrocytes help neurons destroy their unwanted mitochondria.
Alpha-secretase does not necessarily pick up the slack when β-secretase cleavage of amyloid precursor protein wanes, a study in primates finds. It suggests APP can be processed in other ways.
Plenty of genetic risk factors for sporadic ALS are still waiting to be found, according to a new meta-analysis of GWAS data.
Mutated huntingtin may stow away in synaptic vesicles to sneak from one neuron to another.
A man lacking ApoE appears to have no cognitive deficits, and his brain and CSF biomarker profiles appear normal. Some claim the findings support ApoE as a rational drug target for AD.
Scientists have turned a yeast heat shock protein into a powerful disaggregase that attacks TDP-43, FUS, and α-synuclein mutants.
A new project to identify factors that allow some carriers of pathogenic mutations to escape their genetic destinies could be applicable to neurodegenerative diseases.
X-ray crystallography reveals secrets of the glutamate receptor.
While mice sleep, neurons sprout synapses to solidify fresh skills, according to a new study. The brain also keeps amyloid-β levels low while we snooze.
An amplification-based test picks up minute amounts of prion protein in the blood of asymptomatic carriers, but researchers wonder whether regulators will want to screen the population.
Belying some earlier reports, a new study finds that grafted dopamine cells continue to innervate neural networks years after transplantation.
Head injury increases one’s chances of future dementia by 60 percent, according to a study in veterans.
Engaging in cognitive activities throughout life staves off decline. It also delays Aβ accumulation, two studies report.
The largest meta-analysis done to date confirms dramatic variability in age at onset of autosomal-dominant Alzheimer's disease overall, but finds mutation type and parental age at onset to be strong predictive modulators.