As new substrates and functions for BACE continue to emerge, scientists worry about adverse effects of blocking the protease.
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 ...
Once branded as a difficult target, β-secretase has become the crowd favorite. But might pharma have to cool its jets?
Thought to be no place for translation, RNA granules that form in “FUSopathies” turn out to host protein synthesis, after all.
Sleeping in an MRI scanner, babies with ApoE4 genotype reveal myelination and structural differences in brain areas affected in people with Alzheimer’s disease.
The NIH releases whole-genome data from the Alzheimer’s Sequencing Project.
Scientists are tweaking immune pathways to scavenge amyloid and curb symptoms in Alzheimer’s mice.
New research reveals fundamental roles for astrocytes and microglia in shaping neural circuits.
A Conference Devoted to Better Engaging Clinical Trial Volunteers Turning to the Internet for Alzheimer’s Trial Volunteers Patient Engagement in Clinical Trials ...
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 ...
Are New Cognitive Tests Ready For Preclinical Trials? Do Tau Tracers Track Cognitive Decline in Disease? Growth Factor Therapy: Safe in Phase 1, Awaiting Efficacy Data Clinical Trials Conference on Alzheimer’s Disease (CTAD) 2013 ...
A gene therapy approach to protect cholinergic neurons appeared safe and seemed to stabilize brain metabolism in a Phase 1 trial of AD patients.
The Internet is poised to play a growing role in recruiting for Alzheimer’s clinical trials.
In the early days of tau brain imaging, neurofibrillary pathology appears to match up with the subtle cognitive decline of presymptomatic Alzheimer’s.
With several microRNAs being overly active in ALS, an antisense therapy to one slows the disease in mice, apparently by reducing neuroinflammation.