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Journal Cover Nature Reviews Neuroscience
  [SJR: 21.499]   [H-I: 309]   [280 followers]  Follow
    
   Full-text available via subscription Subscription journal
   ISSN (Print) 1471-003X - ISSN (Online) 1471-0048
   Published by NPG Homepage  [124 journals]
  • How can brain mapping initiatives cooperate to achieve the same goal'
    • Authors: Hideyuki Okano, Tetsuo Yamamori
      Pages: 733 - 734
      Abstract: The independent worldwide brain-research initiatives should collaborate in order to enable them to reach their shared goal: gaining a better understanding of the tremendous complexity of the human brain.
      Citation: Nature Reviews Neuroscience 17, 733 (2016)
      PubDate: 2016-09-22
      DOI: 10.1038/nrn.2016.126
      Issue No: Vol. 17, No. 12 (2016)
       
  • How do we know what we know' Discovering neuroscience data sets
           through minimal metadata
    • Authors: Sean L. Hill
      Pages: 735 - 736
      Abstract: With the emergence of brain research initiatives around the world, the need for standards to facilitate neuroscience data sharing is growing. A crucial first step will be to establish a minimal metadata standard that allows the discovery of and access to similar or related data
      Citation: Nature Reviews Neuroscience 17, 735 (2016)
      PubDate: 2016-10-13
      DOI: 10.1038/nrn.2016.134
      Issue No: Vol. 17, No. 12 (2016)
       
  • Neural circuits: Cortical replacements
    • Authors: Darran Yates
      Pages: 737 - 737
      Abstract: Transplanted embryonic neurons can functionally replace ablated neurons in the primary visual cortex in adult mice.
      Citation: Nature Reviews Neuroscience 17, 737 (2016)
      PubDate: 2016-11-17
      DOI: 10.1038/nrn.2016.160
      Issue No: Vol. 17, No. 12 (2016)
       
  • Neurodegenerative disease: Straining the brain
    • Authors: Darran Yates
      Pages: 738 - 738
      Abstract: Following injection into the brain, different strains of tau aggregates induce different presentations of tau neuropathology in a mouse model of tauopathy.
      Citation: Nature Reviews Neuroscience 17, 738 (2016)
      PubDate: 2016-11-17
      DOI: 10.1038/nrn.2016.161
      Issue No: Vol. 17, No. 12 (2016)
       
  • Behavioural neuroscience: Descending into dishonesty
    • Authors: Natasha Bray
      Pages: 738 - 738
      Abstract: Reductions in the response of the amygdala to dishonesty predict the escalation of self-serving dishonesty.
      Citation: Nature Reviews Neuroscience 17, 738 (2016)
      PubDate: 2016-11-10
      DOI: 10.1038/nrn.2016.157
      Issue No: Vol. 17, No. 12 (2016)
       
  • Sleep and memory: Rippling memories
    • Authors: Sian Lewis
      Pages: 739 - 739
      Abstract: Transient, high-frequency hippocampal oscillations called sharp wave–ripples may be involved in the formation of memories that are later consolidated in the neocortex. Oscillations of ripple frequency (∼200 Hz) have been reported in the rodent neocortex during sleep but are not well understood. Here, the authors
      Citation: Nature Reviews Neuroscience 17, 739 (2016)
      PubDate: 2016-11-04
      DOI: 10.1038/nrn.2016.154
      Issue No: Vol. 17, No. 12 (2016)
       
  • Neurodegenerative disease: Resisting the chop
    • Authors: Sian Lewis
      Pages: 739 - 739
      Abstract: It is currently unclear which forms of the protein tau contribute to Alzheimer disease (AD) pathology, but Δtau314, which is produced following caspase 2-mediated tau cleavage, is elevated in the brains of cognitively impaired mice and humans with AD. Here, in vitro expression of
      Citation: Nature Reviews Neuroscience 17, 739 (2016)
      PubDate: 2016-11-04
      DOI: 10.1038/nrn.2016.153
      Issue No: Vol. 17, No. 12 (2016)
       
  • Neural development: The river runs through it
    • Authors: Sian Lewis
      Pages: 739 - 739
      Abstract: In humans, some neurons can be detected migrating after birth from the subventricular zone (SVZ) to cortical regions; however, it is not known to what extent these cells mature and become integrated into human forebrain circuits. Here, brain imaging and time-lapse confocal microscopy were used
      Citation: Nature Reviews Neuroscience 17, 739 (2016)
      PubDate: 2016-11-04
      DOI: 10.1038/nrn.2016.152
      Issue No: Vol. 17, No. 12 (2016)
       
  • Neurodegenerative disease: Actin up
    • Authors: Sian Lewis
      Pages: 739 - 739
      Abstract: The GGGGCC (G4C2) repeat expansion in the C9orf72 gene is a common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), but the mechanism is unknown. Using quantitative proteomics, the authors found that C9orf72 protein interacts with the actin-binding protein cofilin. Cofilin
      Citation: Nature Reviews Neuroscience 17, 739 (2016)
      PubDate: 2016-11-04
      DOI: 10.1038/nrn.2016.151
      Issue No: Vol. 17, No. 12 (2016)
       
  • Neural circuits: Halting hunger
    • Authors: Darran Yates
      Pages: 740 - 740
      Abstract: Cholinergic neurons in the basal forebrain of mice influence the intake of food and body weight by regulating appetite suppression.
      Citation: Nature Reviews Neuroscience 17, 740 (2016)
      PubDate: 2016-11-04
      DOI: 10.1038/nrn.2016.156
      Issue No: Vol. 17, No. 12 (2016)
       
  • Synaptic plasticity: Spinal signals
    • Authors: Katherine Whalley
      Pages: 740 - 740
      Abstract: This study suggests that brain-derived neurotrophic factor (BDNF) is released from dendritic spines in response to activity and acts in an autocrine manner to mediate structural plasticity of the spine from which it was released.
      Citation: Nature Reviews Neuroscience 17, 740 (2016)
      PubDate: 2016-10-20
      DOI: 10.1038/nrn.2016.148
      Issue No: Vol. 17, No. 12 (2016)
       
  • Addiction: Under a stressful influence
    • Authors: Natasha Bray
      Pages: 741 - 741
      Abstract: In rats, stress promotes alcohol use by altering chloride gradients across the membranes of GABAergic neurons in the ventral tegmental area.
      Citation: Nature Reviews Neuroscience 17, 741 (2016)
      PubDate: 2016-10-27
      DOI: 10.1038/nrn.2016.149
      Issue No: Vol. 17, No. 12 (2016)
       
  • Integrins in synapse regulation
    • Authors: Yun Kyung Park, Yukiko Goda
      Pages: 745 - 756
      Abstract: Integrins are a large family of extracellular matrix (ECM) receptors. In the developing and adult brain, many integrins are present at high levels at synapses. The tetrapartite structure of synapses — which comprises presynaptic and postsynaptic neurons, the ECM and glial processes — places synaptic
      Citation: Nature Reviews Neuroscience 17, 745 (2016)
      PubDate: 2016-11-04
      DOI: 10.1038/nrn.2016.138
      Issue No: Vol. 17, No. 12 (2016)
       
  • The mirror mechanism: a basic principle of brain function
    • Authors: Giacomo Rizzolatti, Corrado Sinigaglia
      Pages: 757 - 765
      Abstract: The mirror mechanism is a basic brain mechanism that transforms sensory representations of others' behaviour into one's own motor or visceromotor representations concerning that behaviour. According to its location in the brain, it may fulfil a range of cognitive functions, including action and emotion understanding.
      Citation: Nature Reviews Neuroscience 17, 757 (2016)
      PubDate: 2016-10-20
      DOI: 10.1038/nrn.2016.135
      Issue No: Vol. 17, No. 12 (2016)
       
  • Keeping it in check: chronic viral infection and antiviral immunity in the
           brain
    • Authors: Katelyn D. Miller, Matthias J. Schnell, Glenn F. Rall
      Pages: 766 - 776
      Abstract: It is becoming clear that the manner by which the immune response resolves or contains infection by a pathogen varies according to the tissue that is affected. Unlike many peripheral cell types, CNS neurons are generally non-renewable. Thus, the cytolytic and inflammatory strategies that are
      Citation: Nature Reviews Neuroscience 17, 766 (2016)
      PubDate: 2016-11-04
      DOI: 10.1038/nrn.2016.140
      Issue No: Vol. 17, No. 12 (2016)
       
  • Network abnormalities and interneuron dysfunction in Alzheimer disease
    • Authors: Jorge J. Palop, Lennart Mucke
      Pages: 777 - 792
      Abstract: The function of neural circuits and networks can be controlled, in part, by modulating the synchrony of their components' activities. Network hypersynchrony and altered oscillatory rhythmic activity may contribute to cognitive abnormalities in Alzheimer disease (AD). In this condition, network activities that support cognition are
      Citation: Nature Reviews Neuroscience 17, 777 (2016)
      PubDate: 2016-11-10
      DOI: 10.1038/nrn.2016.141
      Issue No: Vol. 17, No. 12 (2016)
       
 
 
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