Studies of heterogeneity in healthy brain aging reveal varying susceptibilities to aging and delayed development, which deepen aging-development understanding and promote prediction and diagnosis of cognitive decline and neurodegenerative diseases.

The pattern of atrophy in Parkinson's disease is consistent with the disease spreading via intrinsic brain networks.

Structural and functional analysis of a recently discovered non-canonical potassium channel family reveals a unique selectivity filter that is exposed to permeating ions only in the conductive state.

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.

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 promising potential of plasma extracellular vesicle synaptic proteins as clinical biomarkers of disease progression in Parkinson's disease has been presented.

Two GAP proteins bound to mitochondria regulate the enyzme Rab7, and thereby the expansion of the isolation membrane during mitophagy, downstream of PINK1 and Parkin, two proteins that are mutated in familial Parkinson's disease.

Advanced machine learning based brain signal decoding of grip-force as a proxy for movement vigor shows Parkinson's disease related performance reduction, suggestive of a loss of cortical vigor encoding in the absence of dopamine.

Constitutive activation of an innate immunity response in mouse brain causes degeneration of dopaminergic neurons, suggesting novel targets for potentially neuroprotective strategies.

The amyloid patterns overlap with the default-mode network, whereas the tau patterns overlap with distinct functional networks and are associated with a loss of anatomical connectivity and multiple cognitive functions.