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In mouse models, a sluggish thalamic reticular nucleus shortens slow-wave sleep. In one model, activating this brain area lengthened the mice's slumber while also reducing their plaque loads.
To find true brain-behavior correlations, a brain-wide association study needs orders of magnitude more people than the dozens typically used in neuroimaging research.
A mouse model that mimics both signature pathologies of Alzheimer disease develops a day-to-day forgetfulness at four months...
Add a new strand to the growing web of relationships among production of the Aβ peptide, regulation of cholesterol and other lipids, oxidative stress, and the death of neurons in Alzheimer's. Researchers believe that Aβ drives an increase in the conversion of...
Eli Lilly and Company announced yesterday that it has halted its Semagacestat γ-secretase inhibitor program...
The fight against Alzheimer disease rallies warriors of many sorts...
Francis Collins announced that $16 million of federal funds would go toward the first-ever therapeutic prevention trial in cognitively healthy people...
Over the past decade, researchers have shifted away from a literal interpretation of Alois Alzheimer’s groundbreaking discovery...
Can an FDA-approved arthritis drug double as a therapy for Alzheimer disease?...
In yesterday’s Neuron, researchers presented fresh in-vivo support for the amyloid hypothesis and bolster the status of the APP protease BACE as the current favorite target for AD therapy development...
Antibodies against extracellular tau block seeding, diminish brain pathology, and may improve cognition in a mouse model.
After veru- and atabecestat, now a third β-secretase inhibitor, by Eli Lilly and AstraZeneca, is being pulled from ongoing Phase 3 trials of symptomatic Alzheimer’s disease.
Two new papers rekindle acrimonious debate about exactly what “loss-of-function” means when it comes to presenilin mutations in Alzheimer’s pathogenesis.
Presenilin 2 resides almost exclusively in late endosomes, multivesicular bodies, and lysosomes, where it generates a pool of aggregation-prone Aβ. Some PS-1 mutations phenocopy this intraneuronal distribution.
The EPOCH trial of verubecestat was halted for lack of efficacy. APECS trial in prodromal AD continues.
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