Changing the mix of extracellular ions can put neurons to sleep and swell the brain interstitial fluid for better solute flow.
Knocking down TIA1 rescues tau pathology and toxicity in cells.
PKCα helps Aβ weaken synapses, and rare mutations in some Alzheimer’s families make the enzyme more active.
Zilkha conference features news on tau toxicity, a leaky blood-brain barrier, and the biology of pericytes.
After years of doubt, leading scientists are growing cautiously excited about the idea that bacteria might seed plaques.
Aβ Oligomers Purified from Human Brain Microbial Hypotheses Intrigue at Zilkha Alzheimer’s Meeting What’s Up With the Vasculature in Dementia? At the third annual Zilkha Symposium, held April 15, 2016, in Los Angeles, scientists from the United States and ...
A comparison of blood proteins between health and dementia uncovers faulty differentiation signaling, which may have harmful effects on neurogenesis.
The gene-editing technology helps validate risk factors of disease and build better disease models.
Search begins for director of £250 million venture.
It was not easy, but it got done—and the catch looks nothing like prior synthetic or mouse versions of these species.
On the heels of news that microglia mediate synaptic loss in Alzheimer’s, researchers report they may do the same in a subtype of FTD caused by progranulin deficiency.
Compared with previously published model lines, these animals develop more features of amyotrophic lateral sclerosis and frontotemporal dementia.
Backtracking of newly synthesized amyloid precursor protein from the Golgi to the ER facilitates APP modification and Aβ production.
C9ORF72 repeats create RNA foci and dipeptide aggregates in mice, but antisense oligonucleotides suppress them.
Two new papers rekindle acrimonious debate about exactly what “loss-of-function” means when it comes to presenilin mutations in Alzheimer’s pathogenesis.
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