The enzyme that collaborates with ubiquitin ligases to promote the release of defective polypeptides from stalled ribosomes in a process named ribosome-associated degradations has been identified as the ATPase Cdc48.

Proteins implicated in Alzheimer’s disease, including amyloid precursor protein and ApoE receptors, interact with each other and with a signalling molecule called agrin to influence the development of the neuromuscular junction.

High-frequency stimulation of the ventromedial prefrontal cortex, which enhances memory and hippocampal neurogenesis, is a novel target for treatment of dementia-related diseases.

A drug-like molecule called ISRIB, which activates the translation initiation factor eIF2B, antagonizes stress responses as diverse as protein misfolding and nutrient deprivation, and restores protein synthesis, enhancing memory.

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.

The AAA-ATPase VCP sustains sarcoplasmic proteostasis, in part, by controlling autophagosome-lysosome fusion and the integrity of a dynamic tubular lysosomal network.

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

The retrograde vesicular trafficking GARP complex, which is mutated in a neurodegenerative disease, is important for sphingolipid homeostasis in yeast and mammalian cells.

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.