Researchers Revel in C9ORF72 Advances at RNA Symposium Profilin-1 Links Cytoskeleton and RNA Aggregation in ALS The Four Stages of TDP-43 Proteinopathy Blocking a MicroRNA Slows Motor Neuron Disease in Mice Glial Cells Refine Neural Circuits Innate Immune ...
A Conference Devoted to Better Engaging Clinical Trial Volunteers Turning to the Internet for Alzheimer’s Trial Volunteers Patient Engagement in Clinical Trials ...
New research reveals fundamental roles for astrocytes and microglia in shaping neural circuits.
Scientists are tweaking immune pathways to scavenge amyloid and curb symptoms in Alzheimer’s mice.
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 ...
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.
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