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.
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.
New methods reveal that complex local splicing variations are more prevalent in animals than previously appreciated, and demonstrate that local splicing variations are relevant for studies of development, gene regulation and neurodegenerative diseases.
Somatically derived genomic mosaicism in the form of increased DNA content and APP copy number in single neurons plausibly has a function in sporadic Alzheimer’s disease and points to functions for single-neuron gene copy number changes.
TrpV1 receptor activation rescues cognition-relevant network dynamics in mouse hippocampus in an acute Alzheimer disease model providing a novel therapeutic target.
