Known for his contributions to the fundamental understanding of the tau protein, Skip Binder leaves his mark on the Alzheimer's field.
The latest data on TREM2 confirm that a variant in the gene associates with AD, and link it to Parkinson’s, brain degeneration, and γ-secretase.
As NIH researchers are preparing to return to their laboratories, Alzheimer's researchers warn about the greater consequences of cutting already limited resources.
Sleeping in an MRI scanner, babies with ApoE4 genotype reveal myelination and structural differences in brain areas affected in people with Alzheimer’s disease.
A new study proposes microtubule-chopping enzymes as the missing link in the cascade of pathology leading from Aβ to tau to neuronal death.
Functional neuroimaging scans can pick up stark neural abnormalities in football players with repeated head injuries before their cognition drops much in executive function tests.
An astrocyte protein stymies toxic interplay between Aβ oligomers and prion proteins.
Changing ApoE levels in midlife influences Aβ pathology in mice, supporting an ApoE-oriented therapeutic strategy in Alzheimer’s disease.
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.