Articles in 2012

Recent improvements in the technology available for the analysis of genetic variability have revolutionized the study of many diseases. Hardy and colleagues illustrate how genome-wide strategies, including whole-genome and whole-exome sequencing, have been used to improve our understanding of the pathobiological mechanisms of neurological diseases

Multiple sclerosis (MS) is generally considered to be an autoimmune, inflammatory disease. In this provocative Perspective, Stys and colleagues propose that non-inflammatory, primary progressive MS is the 'real' MS, and that inflammatory forms of the disorder reflect an aberrant immune reaction to ongoing cytodegeneration.

Functional MRI studies have revealed useful information about the ageing brain. In this Review, Cheryl Grady explains how correlating cognitive decline to changes in brain structure and function is hampered by the complexity of the ageing process.

Behavioural learning is accompanied by loss and gain of synapses, which is thought to be the mechanism by which circuits are altered and 'memory traces' established. Recent research, reviewed here, suggests that learning and memory events involve the rearrangement of ensembles of adjacent synapses on short stretches of dendrites.

A cytoskeleton in the distal part of the axon forms a boundary that spatially restricts AnkG clustering and thereby AIS assembly.

Transplanted forebrain interneuron precursors integrate into spinal cord circuits and relieve neuropathic pain symptoms.

The microRNA let-7 can induce neurodegeneration by activating the Toll-like receptor TLR7.

A single exposure to a shock wave associated with a 'typical' explosive device is sufficient to induce sustained brain pathology and memory impairments as early as 2 weeks after exposure in mice.

Tryptophan metabolism along the kynurenine pathway generates several neuroactive metabolites. Schwarcz and colleagues discuss the regulation of this pathway in the normal brain and in neurological and psychiatric disorders, and consider the potential therapeutic opportunities of targeting this pathway.

ARC targets less active synapses for weakening through an interaction with inactive CaMKIIβ.

Diabetic patients often experience chronic pain as a complication of their condition. In this study, a metabolite produced under hyperglycaemic conditions is shown to influence the function of voltage-gated sodium channels expressed in nociceptive neurons resulting in neuropathic pain.