G8 Vows to Improve Care, Cure Dementia
G8 leaders set 2025 as their goal to find better treatment for Alzheimer's and vowed to coordinate research and care strategies.
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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.
New research suggests that TDP-43 attacks neurons by deactivating a translation initiation factor. Keeping the factor active holds toxicity at bay in flies.
Researchers at BACE meeting explore how trafficking and degradation of the protease relate to amyloid pathology in AD.
By stopping familial amyloid polyneuropathy in its tracks, a repurposed anti-inflammatory medication supports the idea that artificial chaperones can prevent protein aggregation.
New research reveals fundamental roles for astrocytes and microglia in shaping neural circuits.