Alzheimer’s Whole-Genome Data Now Available From the NIH
The NIH releases whole-genome data from the Alzheimer’s Sequencing Project.
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The NIH releases whole-genome data from the Alzheimer’s Sequencing Project.
Thought to be no place for translation, RNA granules that form in “FUSopathies” turn out to host protein synthesis, after all.
Once branded as a difficult target, β-secretase has become the crowd favorite. But might pharma have to cool its jets?
Cloistered Retreat Takes the Pulse of BACE Research BACE—Substrates, Functions, Developmental Phenotypes Blocking BACE—Do Adult Mouse Phenotypes Predict Side Effects? Meeting Explores Complex Biology of BACE Regulation BACE Proteases in Health and Disease
As new substrates and functions for BACE continue to emerge, scientists worry about adverse effects of blocking the protease.
A European public-private partnership plans to combine faster enrollment with adaptive trials to hasten drug discovery in Alzheimer's.
European Project Mixes Adaptive Design with Trial-Ready Cohort G8 Vows to Improve Care, Cure Dementia G8 Dementia Summit
G8 leaders set 2025 as their goal to find better treatment for Alzheimer's and vowed to coordinate research and care strategies.
Researchers at a meeting on BACE shared concerns that blocking the protease in adults might have unexpected consequences.
Exome sequencing identifies a new Alzheimer’s risk gene—phospholipase D3.
A small panel of fluid biomarkers could predict a slow or fast disease course in amyotrophic lateral sclerosis.
First-generation γ-secretase modulators are less potent in human neurons than in some other cell types, possibly explaining why these drugs failed in clinical trials.
Merck’s BACE inhibitor has survived its most recent safety evaluation and will undergo more testing in two trials—one for mild to moderate Alzheimer's, the other for mild cognitive impairment due to AD.
The protein that causes progeria, the accelerated aging disease, hastens pathology in neurons derived from people with Parkinson's.
A new study proposes that two genetic risk factors for frontotemporal dementia interact, disrupting brain connectivity decades before symptoms.