Combining exome sequencing with gene interaction analysis allowed researchers to identify 18 new genes for an inherited movement disorder. This method could lead to genes linked to other neurodegenerative diseases.
Researchers have sliced and digitally reassembled a famous brain in neuroscience to view its detailed three-dimensional architecture.
Scientists claim to turn differentiated mouse cells into pluripotent ones with a brief dip in an acid bath—no genetic tweaks necessary.
Using the transferrin receptor to deliver therapeutics to the brain is tricky—antibodies that bind too tightly stall in blood vessel cells and shut down transport.
A small study suggests that exposure to the pesticide DDT heightens the risk of developing Alzheimer’s disease.
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.
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.