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Preview: Nature Neuroscience - Issue - science feeds

Nature Neuroscience - Issue - science feeds

Nature Neuroscience offers a unique mix of opinion and reviews alongside top-quality research papers. Published monthly, in print and online, the journal reflects the entire spectrum of neuroscience, from molecular to cognitive.


Focus on psychiatric disorders


Nature Neuroscience presents a Focus issue highlighting progress in basic and clinical sciences advancing mental health research.

Back to basics: luring industry back into neuroscience


An obsession with producing and validating models (face, construct, predictive validity) has led many of us down a deep rabbit hole, thinking about models instead of mechanisms. Advances in the human genetics and neurobiology of brain disorders creates exciting new opportunities, but only if we can get back to basics.

On being a circuit psychiatrist


Recent technological advancements in the study of neural circuits provide reasons to be optimistic that novel treatments for psychiatric illnesses are just around the corner. Maximizing the chances of translating these advancements into real improvements in patient care requires a carefully considered road map.

Psychiatric distress in animals versus animal models of psychiatric distress


Primatology research suggests that other primates suffer from crippling depression or anxiety, implying that these diseases' roots pre-date human history. At the same time, some realms of psychiatry remain uniquely human. Recognizing the similarities and dissimilarities between us and other primates is essential in studying animal models of psychiatric disease.

The origin and natural history of autism spectrum disorders


Refined social phenotyping of syndromic and idiopathic forms of autism, combined with advances in genetics, animal models of syndromes and brain imaging, may facilitate discovery of shared brain mechanisms that will lead to new treatments. The reversal of social deficits in animal models is promising for eventual translation into therapeutics.

Translating genome-wide association findings into new therapeutics for psychiatry


The Psychiatric Genomics Consortium is aiming to analyze data from >1 million individuals. This is already leading to hundreds of new genetic findings across psychiatric disorders with the potential to restart largely stalled psychiatric drug development pipelines. This paper outlines key questions and plans to translate findings into new therapeutics.

The road to precision psychiatry: translating genetics into disease mechanisms


Recently, robust identification of hundreds of genetic variants associated with risk for neuropsychiatric disease has prompted new challenges in understanding their biological impact within an individual. The authors provide a framework for interpretation of genetic risk variants to uncover disease mechanisms and facilitate therapeutic development.

Lessons learned from studying syndromic autism spectrum disorders


Autism spectrum disorders are highly heterogeneous and include both idiopathic and syndromic forms. Sztainberg and Zoghbi discuss insights gained from studying syndromic autism spectrum disorders and their potential contribution to our understanding of the molecular pathways critical for normal cognitive and social development, as well as the relevance to idiopathic autism.

Using model systems to understand errant plasticity mechanisms in psychiatric disorders


Animal models have failed to yield new treatments for psychiatric disorders. Some psychiatric disorders may result from pathology in plasticity mechanisms. Therefore, understanding plasticity mechanisms in model systems may provide insight into the disordered processes in patients.

Rare variants are common in schizophrenia


A large DNA sequencing study of schizophrenia finds more evidence that rare inherited coding mutations across many genes contribute to risk of the disorder. This has important implications for geneticists and neuroscientists alike.

Brains, genes and power


Gene expression data from more than 500 human brains shed light on the molecular consequences of genetic variation that contributes to schizophrenia.

When size matters: CHD8 in autism


Recent models studying loss of the mouse homolog of the autism-associated gene CHD8 show altered Wnt signaling, cell fate and proliferation. How do these findings shape our understanding of this disease?

Increased burden of ultra-rare protein-altering variants among 4,877 individuals with schizophrenia


Using whole-exome sequencing, the authors identified 244,246 coding-sequence and splice-site ultra-rare variants (URVs) and found that gene-disruptive and putatively protein-damaging URVs were significantly more abundant in schizophrenia cases than in controls. The excess of protein-compromising URVs was concentrated in brain-specific genes, particularly in neuronally expressed genes whose proteins are located at the synapse.

Gene expression elucidates functional impact of polygenic risk for schizophrenia


The CommonMind Consortium sequenced RNA from dorsolateral prefrontal cortex of subjects with schizophrenia (N = 258) and control subjects (N = 279), creating a resource of gene expression and its genetic regulation. Using this resource, they found that ∼20% of schizophrenia loci have variants that may contribute to altered gene expression and liability.

Genome-wide prediction and functional characterization of the genetic basis of autism spectrum disorder


Autism spectrum disorder is a complex disease with a strong genetic basis that remains under-characterized by current genetics studies. Here, the authors use a computational approach based on a human brain-specific gene network to predict autism-associated genes across the genome and further delineate their functional and developmental characteristics.

Genome-wide, integrative analysis implicates microRNA dysregulation in autism spectrum disorder


The authors performed genome-wide microRNA (miRNA) expression profiling in post-mortem brains from individuals with autism spectrum disorder (ASD) and controls, and identified miRNAs and co-regulated modules perturbed in ASD.

Chd8 mediates cortical neurogenesis via transcriptional regulation of cell cycle and Wnt signaling


De novo mutations in CHD8 are associated with autism spectrum disorder, but the basic biology of CHD8 remains poorly understood. Here the authors find that Chd8 knockdown during cortical development results in defective neural progenitor proliferation and differentiation that ultimately manifests in abnormal neuronal morphology and behaviors in adult mice.

Ucn3 and CRF-R2 in the medial amygdala regulate complex social dynamics


Social encounters are associated with varying degrees of stress. The authors show that modulation of stress system components in the medial amygdala alters preference for familiar vs. novel conspecifics. Inhibition of the relevant circuit in a group of familiar mice kept under semi-natural conditions increased pro-social behavior.

Histone deacetylase 3 associates with MeCP2 to regulate FOXO and social behavior


Mutations in MECP2 cause Rett syndrome. The authors show that a MeCP2-HDAC3 complex positively regulates a subset of neuronal genes through FOXO recruitment and deacetylation, and that HDAC3 loss contributes to cognitive and social deficits in mice. Rett-patient-derived cells exhibited similar HDAC3-FOXO-mediated transcriptional impairments and were rescued by gene editing.

MeCP2 and histone deacetylases 1 and 2 in dorsal striatum collectively suppress repetitive behaviors


Loss of Hdac1 and Hdac2 in adult brain is detrimental to neuronal survival and triggers dysregulation of Sapap3 in the striatum in a MeCP2-dependent manner that results in an exacerbated repetitive behavior phenotype.

Foxp2 controls synaptic wiring of corticostriatal circuits and vocal communication by opposing Mef2c


Chen et al. found that Foxp2 interacts with Mef2c to wire synaptic circuits linking neocortex to basal ganglia. The study analyzes the basics of circuit wiring underlying vocal communication.

Multimodal population brain imaging in the UK Biobank prospective epidemiological study


The UK Biobank combines detailed phenotyping and genotyping with tracking of long-term health outcomes in a large cohort. This study describes the recently launched brain-imaging component that will ultimately scan 100,000 individuals. Results from the first 5,000 subjects are reported, including thousands of associations, population modes and hypothesis-driven results.