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 ...
Researchers at a meeting on BACE shared concerns that blocking the protease in adults might have unexpected consequences.
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.
New research suggests that TDP-43 attacks neurons by deactivating a translation initiation factor. Keeping the factor active holds toxicity at bay in flies.
By stopping familial amyloid polyneuropathy in its tracks, a repurposed anti-inflammatory medication supports the idea that artificial chaperones can prevent protein aggregation.
Alzforum’s summary of research highlights of 2013.
Vitamin E slows functional deterioration in people with mild to moderate Alzheimer's disease, according to a new study.
Evidence builds that amyotrophic lateral sclerosis and frontotemporal lobar degeneration sit on the same pathological spectrum, but scientists are unsure how the disease marker TDP-43 fits in.
A combination of high clusterin and low Aβ42 in cerebrospinal fluid associates with early Alzheimer’s neurodegeneration, hinting at a mechanistic interaction between the proteins.