Government, industry, and advocacy together will provide nearly $130 million for the identification of surrogate markers and targets.
Mutant FUS meddles with RNA splicing and DNA damage repair in transgenic mice that succumb to disease.
The antidepressant citalopram reduces agitation in Alzheimer’s patients, but caused abnormal heart rhythms at the tested dose.
The amyloid imaging agent florbetapir predicts cognitive decline much like its forerunner, PiB.
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.
Superficial siderosis, a leakage of blood matter onto the outer surface of the cerebral cortex, may be linked to AD and other dementias.
Amyotrophic lateral sclerosis may be inherited more often than previously believed, prompting neurologists to rethink how they define familial versus sporadic disease.
The 2014 U.S. budget increases Alzheimer’s research funding by $80 million, offsetting some of the damage done by the 2013 sequestration.
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.
Misfolded TDP-43 spreads along defined pathways in Alzheimer’s and frontotemporal dementia, tracing axonal routes between neurons.
The National Institutes of Health is testing pilot initiatives to address the problem of irreproducible scientific results.
Taking down a cellular henchman linked to a cell death pathway relieves symptoms of a lysosomal storage disorder in mice. Researchers hope the pathway could lead to a treatment.