Scientists are trying to help the brain replace lost dopamine in people with Parkinson's. Will gene therapy or cell replacement work eventually?
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.
Neuroligin, a synapse-building protein previously tied to autism, may play a part in Alzheimer’s disease through neuroinflammation and DNA transcription.
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.
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.
Scientists claim to turn differentiated mouse cells into pluripotent ones with a brief dip in an acid bath—no genetic tweaks necessary.
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.
Proteins that interact with the Parkinson’s risk gene LRRK2 point to protein trafficking and degradation as causes of pathogenesis.
Once considered a nuclear homebody, TDP-43 ventures out to accompany mRNAs down axons to nerve terminals where the transcripts can be turned into protein.
Aggressively treating high blood pressure and cholesterol in older adults with diabetes does not prevent cognitive decline, and results in more brain shrinkage.
Live imaging of the mouse brain offers a rare view of α-synuclein dynamics at presynaptic terminals, and raises questions about which form of the protein triggers synaptic dysfunction.