Identification of causal genes and their effects on other biological determinants untangles the complexities of aging and Alzheimer's and can facilitate drug discovery for sustaining healthy aging and treating Alzheimer's.
White matter microstructure alterations in key bundles affected in Alzheimer's disease are related to amyloid and tau pathology in the preclinical phase of sporadic and autosomal-dominant Alzheimer's disease.
BIN1 forms a complex with Tau and voltage-gated calcium channels in neurons, and higher BIN1 levels promote neuronal activity, calcium influx, and bursting that is blocked by reducing Tau.
Neuronal ELAV-like (nELAVL) proteins are associated with non-coding Y RNAs in stressed neurons and in the brains of Alzheimer's disease patients, suggesting a new means of regulatory protein sequestration and mRNA target regulation.
An internet-based cohort study of paired associate learning shows that a first-degree family history of dementia is associated with lowered performance, an effect modified by apolipoprotein E genotype and diabetes.
A massively parallel analysis of the effects of mutations on amyloid beta nucleation provide the first comprehensive atlas of how mutations alter the formation of amyloid fibrils.
Visual narrow-band gamma rhythms are reduced in mild cognitive impairment and Alzheimer’s disease, confirming previous rodent research and forming crucial first steps for development of EEG-based biomarkers for humans.
Increased excitation and decreased inhibition associated with abnormal neuronal morphology, aberrant ion channel properties, and synaptic dysfunction contribute to hyperexcitability in Alzheimer’s disease hiPSC-derived neuronal cultures and cerebral organoids.
Increased levels of brain Hebp1 starting from the presymptomatic stage of Alzheimer’s disease contributes to progressive neuronal loss by triggering mitochondrial-dependent apoptosis in neurons exposed to elevated heme.
