Articles in 2015

Fragile X syndrome (FXS) results from the loss of the RNA-binding protein fragile X mental retardation protein (FMRP). Here, Klann and colleagues discuss the ways in which FMRP loss disrupts mRNA translation in the brain and the outcomes of genetic and pharmacological attempts to reset translational homeostasis in FXS model mice.

Neuronal atrophy early in a mouse model of spinal cerebellar ataxia 1 may represent an adaptive mechanism that restores the density of potassium channels in Purkinje neurons, thus normalizing membrane polarization and firing.

Activity-dependent redistribution of cadherin–catenin complexes between neighbouring dendritic spines drives pruning versus maturation.

Neutrophil infiltration of the brain drives cognitive decline in mouse models of Alzheimer disease and is regulated by the integrin LFA-1.

Memory storage is thought to be mediated by lasting physical changes, or engrams, in the brain. In this Review, Josselyn and colleagues discuss characteristics of the engram and describe the recent progress that has been made in identifying neurons involved in specific engrams.

Schizophrenia is characterized by various neurocognitive deficits, including impairments in auditory function. In this Review, Javitt and Sweet examine the behavioural, neurophysiological and structural evidence for auditory cortical dysfunction in this disorder and explore some of the possible underlying mechanisms.

Recent years have seen considerable interest in the genetics of autism spectrum disorder (ASD). In this Review, Thomas Bourgeron examines the genetic architecture of this disorder and how ASD-linked mutations might affect synaptic plasticity, before exploring the synaptic homeostasis hypothesis of ASD.

Presynaptic β-neurexins regulate synaptic strength at excitatory synapses by modulating endocannabinoid signalling.

A new study identifies a population of 'speed cells' in the rat medial entorhinal cortex that is likely to contribute to path integration.

Individuals with Down syndrome have an enhanced risk of developing early onset Alzheimer disease. Here, the authors describe the features of Alzheimer disease in Down syndrome and show how understanding the genetic and pathogenic mechanisms of this form of Alzheimer disease may shed light on more general mechanisms of neurodegeneration.

Emerging evidence suggests a role for the voltage-gated sodium channel Na_V1.9 in pain. In this Progress article, Dib-Hajj, Black and Waxman analyse the findings from three studies that report mutations in the gene encoding Na_V1.9 in pain disorders, and suggest that Na_V1.9 may be a potential therapeutic target for pain.