Excitatory and inhibitory neuronal abnormalities show distinct associations to tau and amyloid accumulations in patients with Alzheimer’s disease.

Impaired GABAergic and glutamatergic synaptic function and loss of interneurons in the amygdala, hippocampus, and cerebellum cause characteristic disease symptoms in a mouse model juvenile neuronal ceroid lipofuscinosis.

Spontaneous fluctuations in pupil-indexed arousal shape human cortical dynamics in a frequency-dependent and spatially diverse manner.

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.

While tau and aging have highly overlapping differential gene expression signatures, they diverge in the affected cell types, with aging having a wide-ranging impact and tau-triggered changes instead polarized to excitatory neurons and glia.

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.

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.

Unbiased computational integration of single-cell- and human genetics data shows that susceptibility to obesity is driven by a broad set of neuronal populations across the brain.

Extracellular vesicles are proposed as novel, non-cell-autonomous mediators of neuronal atrophy in Parkinson's disease.

Identification of activity-dependent transcriptional changes in striatal neurons reveals a conserved functional enhancer for prodynorphin.