Discovery of a physiological LRRK2 substrate and a new mechanism of Rab regulation should aid Parkinson’s research and the understanding of Rab function.

Although cellular organelles show a functional deterioration in aging, genetic loci associated with common age-associated disease instead nominate nuclear transcription factors across several age-related diseases.

The spiking activity of the subthalamic nucleus, rather than the activity of striatal projection neurons, orchestrates basal ganglia downstream activity and output commands in health and Parkinson’s disease.

A comprehensive resource to systematically evaluate the genetically predicted associations between 125 polygenic risk scores and 249 metabolic traits.

The ATP7A interactome is the first comprehensive view of putative Menkes disease neurodegeneration mechanisms.

Standing genetic variation for disease resistance may be continuously lost during recurring warm water episodes because of widespread susceptibility of disease-resistant genotypes to bleaching and the independence between these two traits.

Convergent screens targeting the levels of alpha-synuclein and tau identify TRIM28 as a driver of their stability, nuclear accumulation and subsequent toxicity.

mTORC1 and c-Jun are implicated in a possible mechanism causing myelin loss downstream of mitochondrial dysfunction in Schwann cells.

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.

Studies in a mouse model of spinocerebellar ataxia type 1 show that a protein called capicua stabilizes toxic ataxin-1 oligomers offering a possible explanation for regional patterns of neurodegeneration.