Protein strains may underlie different tauopathies, according to researchers presented at this year's AAIC meeting in Boston.
Meet ADCS-PACC, C3: Composites that measure subtle changes in cognition appear reliable, clearing the way for their use in clinical trials of people with presymptomatic AD.
With several microRNAs being overly active in ALS, an antisense therapy to one slows the disease in mice, apparently by reducing neuroinflammation.
A new study proposes that two genetic risk factors for frontotemporal dementia interact, disrupting brain connectivity decades before symptoms.
New research suggests that TDP-43 attacks neurons by deactivating a translation initiation factor. Keeping the factor active holds toxicity at bay in flies.
By stopping familial amyloid polyneuropathy in its tracks, a repurposed anti-inflammatory medication supports the idea that artificial chaperones can prevent protein aggregation.
Early dysfunction in Alzheimer’s may start in the lateral entorhinal cortex and spread from there to connected cortical brain regions.
Vitamin E slows functional deterioration in people with mild to moderate Alzheimer's disease, according to a new study.
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.
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.
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.
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.