The combination of deep learning with whole-brain computational models reveals the low-dimensional representation of neurodegenerative diseases, which emerges from a highly multidimensional brain, providing valuable insight into pathological states' diagnostic, prognosis, and treatment response.

Simply crushed zizyphi spinosi semen not only ameliorates Aβ, tau, and α-synuclein pathology in dementia model mice, but also rejuvenates brain function by suppressing cellular senescence in normal aged mice.

Structural, biophysical, and functional analyses reveal that mutations in TREM2 trigger either misfolding or reduced binding to cell-surface glycosaminoglycans, which segregate with neurodegenerative disease link and highlight a functional surface linked to the pathogenesis of Alzheimer's disease.

Computational-driven, imaging-based topological profiles of neurodegeneration differ substantially in different neurodegenerative conditions, suggesting distinct modes of dependence of the pathological spread on the underlying connectivity.

When non-glycosylated, Seipin, which spans the endoplasmic reticulum (ER) membrane twice, forms aggregates in an oligomerization-dependent manner, distorts the shape of the ER, and incorporates SERCA2b via direct interaction, inactivation of which results in induction of ER stress and apoptosis.

STOMP is a technique that can determine the proteomic composition of any feature that is identifiable by laser scanning microscopy and is at least one cubic micron in size.

A lack of ADAM10-mediated shedding increases prion protein levels at the plasma membrane and promotes the generation of pathological prion proteins, which accelerates prion disease in mice.

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

Major cell types across various brain regions distinctively associate with tissue loss in 13 neurodegenerative conditions.

Local brain functional activity reductions in bvFTD follow the distribution of serotonergic, GABAergic, and norepinephrinergic neurotransmitter systems, indicating a selective vulnerability and providing novel insights into the underlying disease mechanisms.