People with neurodegeneration but not brain amyloid surface in two new studies of preclinical AD, suggesting this odd population is both legitimate and potentially large.
Changing ApoE levels in midlife influences Aβ pathology in mice, supporting an ApoE-oriented therapeutic strategy in Alzheimer’s disease.
Allegations of falsified data embroil Japanese ADNI; project leaders respond that data corrections followed quality-control procedures.
Protein strains may underlie different tauopathies, according to researchers presented at this year's AAIC meeting in Boston.
Removing a key component of the innate immune system worsens amyloid deposition but improves memory in mice that model Alzheimer's pathology.
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.