The National Institutes of Health is testing pilot initiatives to address the problem of irreproducible scientific results.
Misfolded TDP-43 spreads along defined pathways in Alzheimer’s and frontotemporal dementia, tracing axonal routes between neurons.
Neuroligin, a synapse-building protein previously tied to autism, may play a part in Alzheimer’s disease through neuroinflammation and DNA transcription.
Data from Phase 3 solanezumab and bapineuzumab trials are formally published. Both missed their primary endpoints, but researchers gleaned insights about Alzheimer’s diagnosis and biomarkers, as well as how to proceed with amyloid immunotherapy therapy.
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.