A new study finds that the cancer drug imatinib does not lower Aβ in humans, casting doubt on a previously described relationship between imatinib, γ-secretase activating protein (GSAP), and Aβ.
Known for his contributions to the fundamental understanding of the tau protein, Skip Binder leaves his mark on the Alzheimer's field.
New data questions whether LRRK2’s kinase activity contributes to Parkinson’s, finding instead that absolute levels of the protein matter more.
Neuroligin, a synapse-building protein previously tied to autism, may play a part in Alzheimer’s disease through neuroinflammation and DNA transcription.
People with previous head injuries may be more prone to amyloid deposition and have a higher risk for Alzheimer's.
Sleeping in an MRI scanner, babies with ApoE4 genotype reveal myelination and structural differences in brain areas affected in people with Alzheimer’s disease.
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.
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.
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.