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.
A Phase 2 trial suggests that the drug PBT2 is generally safe for Huntington’s patients. The drug's sponsor says it may have improved cognition, though experts remain unconvinced.
Researchers identify a transcription factor that protects neurons during normal aging but goes AWOL in Alzheimer’s brains.
Allegations of falsified data embroil Japanese ADNI; project leaders respond that data corrections followed quality-control procedures.
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.
A transcription factor thought to mark stressed-out motor neurons activates genes that help them survive. It maintains muscle mass, but not strength.
A small study suggests that exposure to the pesticide DDT heightens the risk of developing Alzheimer’s disease.
Researchers have sliced and digitally reassembled a famous brain in neuroscience to view its detailed three-dimensional architecture.
Government, industry, and advocacy together will provide nearly $130 million for the identification of surrogate markers and targets.
Superficial siderosis, a leakage of blood matter onto the outer surface of the cerebral cortex, may be linked to AD and other dementias.
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.
Amyotrophic lateral sclerosis may be inherited more often than previously believed, prompting neurologists to rethink how they define familial versus sporadic disease.
People with previous head injuries may be more prone to amyloid deposition and have a higher risk for Alzheimer's.