Unaffected members of families with a history of late-onset Alzheimer’s disease have an increased risk of progressing to the disease, a new study confirms.
The 2014 U.S. budget increases Alzheimer’s research funding by $80 million, offsetting some of the damage done by the 2013 sequestration.
Scientists are trying to help the brain replace lost dopamine in people with Parkinson's. Will gene therapy or cell replacement work eventually?
A transcription factor thought to mark stressed-out motor neurons activates genes that help them survive. It maintains muscle mass, but not strength.
Allegations of falsified data embroil Japanese ADNI; project leaders respond that data corrections followed quality-control procedures.
New data questions whether LRRK2’s kinase activity contributes to Parkinson’s, finding instead that absolute levels of the protein matter more.
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.