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.
People with previous head injuries may be more prone to amyloid deposition and have a higher risk for Alzheimer's.
Amyotrophic lateral sclerosis may be inherited more often than previously believed, prompting neurologists to rethink how they define familial versus sporadic disease.
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.
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.
Vitamin E slows functional deterioration in people with mild to moderate Alzheimer's disease, according to a new study.
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.