Functional genomics and mouse analyses blame waning levels of histone-binding protein for memory loss in aging.
Brain connections weaken years before cognition in sporadic and familial Alzheimer’s.
Is transfer of tau from one neuron to the next a normal activity, hijacked by pathogenic protein in the case of tauopathies?
Expansions in ataxin-2 can lead to either ALS or spinocerebellar ataxia—even in the same family, according to a new pedigree from New York.
Studies support the idea that mitochondrial changes drive aging and AD pathogenesis.
Two studies examine factors that heighten the risk for dementia in type 2 diabetes patients. Both highlight depression as a dangerous comorbidity.
A parkinsonism-associated ubiquitin ligase interacts with parkin to promote mitophagy.
Researchers identified a genetic variant in the microglial gene CD33 that protects against Alzheimer’s.
Alzheimer’s and prion disease may be linked through an α-secretase.
The route to early dementia starts in adolescence, with low cognitive function and alcohol intoxication as major predictors.
Studies reported at AAIC demonstrate that biomarkers help predict who will develop cognitive impairment and dementia.
AD but no Amyloidβ? Researchers at AAIC 2013 theorized on the pathology underlying this form of dementia.
Cerebrospinal Fluid Tau Climbs in Aβ Mouse Models Coverage Denial For Amyloid Scans Riles Alzheimer’s Community Pooled GWAS Reveals New Alzheimer’s Genes and Pathways Are Subtle Memory Concerns a Sign of Future Dementia? Clinical Trials Roundup: Four Hits ...
Motor and cortical neurons are particularly vulnerable to FUSopathy. A new paper suggests they fail because they depend strongly on FUS to regulate transcription.
Activating translation regulator eIF2alpha restores plasticity and memory in Alzheimer's models.