Articles in 2017

Hypothalamic neural stem cells may be important regulators of the speed at which ageing proceeds in mice.

Non-coding RNAs (ncRNAs) have been implicated in the pathophysiology of various neurodegenerative diseases. In this Review, Salta and De Strooper discuss the mechanisms by which ncRNAs may be linked to neurodegeneration and touch on the use of ncRNA-based biomarkers and therapies for these conditions.

Several of the spinocerebellar ataxias (SCAs) result from expansion of polyglutamine (polyQ)-encoding regions in different genes. Here, Orr and colleagues examine the clinical features of the the polyQ SCAs, and suggest that understanding the molecular and physiological mechanisms underlying polyQ SCAs can inform therapeutic strategies for these and other polyQ disorders.

The likelihood of winning a bout of competitive behaviour is increased by past wins, and the neural circuitry underlying this crucial determinant of social rank in a group of mice is identified as a projection from the mediodorsal thalamus to the dorsomedial prefrontal cortex.

Attempts to group the cells of the nervous system into classes or types face technical and conceptual barriers. Zeng and Sanes consider the current approaches to classification and propose a strategy and set of principles to guide future classification efforts.

This study provides evidence for a role for the thalamus in the synchronization of brain rhythms that drive memory consolidation during sleep.

Two major components of depression-like behaviour in mice — social avoidance and helplessness — are mediated by distinct circuits that include parvalbumin-expressing neurons in the ventral pallidum.

In mice, hypothalamic agouti-related peptide-expressing neurons modulate food-cue-associated insular cortex activity to influence behaviour.

The development of chronic neuropathic pain is associated with cortical hyperexcitability and a marked decrease in inhibition, particularly from cortical somatostatin-expressing interneurons.

Enterochromaffin cells in the gut epithelium act as chemosensors and can modulate neural function in response to intestinal signals.

The aggregation of α-synuclein in neurons is characteristic of Parkinson disease. Koprich, Kalia and Brotchie provide a critical overview of preclinical, mammalian models of α-synucleinopathy and their merits and limitations in drug development for Parkinson disease, and suggest a combination of different models for optimal proof-of-principle investigation of novel therapeutics.