A new study finds that the cancer drug imatinib does not lower Aβ in humans, casting doubt on a previously described relationship between imatinib, γ-secretase activating protein (GSAP), and Aβ.
Alzforum’s summary of research highlights of 2013.
Early dysfunction in Alzheimer’s may start in the lateral entorhinal cortex and spread from there to connected cortical brain regions.
By stopping familial amyloid polyneuropathy in its tracks, a repurposed anti-inflammatory medication supports the idea that artificial chaperones can prevent protein aggregation.
Researchers at BACE meeting explore how trafficking and degradation of the protease relate to amyloid pathology in AD.
In neurodegenerative disease, tau is in the dendrites, and scientists are beginning to flesh out ways to block what it does there.
New research suggests that TDP-43 attacks neurons by deactivating a translation initiation factor. Keeping the factor active holds toxicity at bay in flies.
New research strengthens the idea that microglia do far more than scour the brain for emergencies.
A new study proposes that two genetic risk factors for frontotemporal dementia interact, disrupting brain connectivity decades before symptoms.
The protein that causes progeria, the accelerated aging disease, hastens pathology in neurons derived from people with Parkinson's.
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.
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.
A small panel of fluid biomarkers could predict a slow or fast disease course in amyotrophic lateral sclerosis.
Exome sequencing identifies a new Alzheimer’s risk gene—phospholipase D3.
Researchers at a meeting on BACE shared concerns that blocking the protease in adults might have unexpected consequences.