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.
New research strengthens the idea that microglia do far more than scour the brain for emergencies.
Early dysfunction in Alzheimer’s may start in the lateral entorhinal cortex and spread from there to connected cortical brain regions.
Researchers have co-opted a molecular transport system to shuttle Aβ antibodies across the mouse blood-brain barrier. They predict the shuttle could smuggle a variety of drugs into the brain.
In neurodegenerative disease, tau is in the dendrites, and scientists are beginning to flesh out ways to block what it does there.
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.
People with previous head injuries may be more prone to amyloid deposition and have a higher risk for Alzheimer's.