Stroke articles within Nature

Featured

  • Article
    | Open Access

    A cross-ancestry meta-analysis of genome-wide association studies identifies association signals for stroke and its subtypes at 89 (61 new) independent loci, reveals putative causal genes, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as potential drug targets, and provides cross-ancestry integrative risk prediction.

    • Aniket Mishra
    • , Rainer Malik
    •  & Stephanie Debette

  • Article |

    Aggressive cerebral cavernous malformations (CCMs) are found to grow through a three-hit cancer-like mechanism, involving gain of function of a gene that promotes vascular growth, and loss of function of genes that suppress it.

    • Aileen A. Ren
    • , Daniel A. Snellings
    •  & Mark L. Kahn

  • Article |

    Lipopolysaccharide derived from gut bacteria can accelerate the formation of cerebral cavernous malformations by activating TLR4 on endothelial cells, and polymorphisms that increase expression of the genes encoding TLR4 or its co-receptor CD14 are associated with higher CCM lesion burden in humans.

    • Alan T. Tang
    • , Jaesung P. Choi
    •  & Mark L. Kahn

  • Letter |

    In a mouse model of ischaemia, mitochondrial particles released from astroctyes are taken up by adjacent neurons, leading to enhanced cell survival signalling; disruption of this release mechanism resulted in worsened neurological outcomes.

    • Kazuhide Hayakawa
    • , Elga Esposito
    •  & Eng H. Lo

  • Letter |

    Ischaemia damages nerve myelin by depriving neurons and their myelinating oligodendrocytes of oxygen and glucose; here it is shown that ischaemic damage is caused through the H+-dependent activation of TRPA1 channels, and not via glutamate receptors of the NMDA type, as previously thought, providing a new mechanism and promising therapeutic targets for diseases as diverse and prevalent as cerebral palsy, spinal cord injury, stroke and multiple sclerosis.

    • Nicola B. Hamilton
    • , Karolina Kolodziejczyk
    •  & David Attwell

  • Outlook |

    New drugs and more focused therapy might cut down on atrial fibrillation and reduce the incidence of stroke.

    • Neil Savage

  • Letter |

    Tat-NR2B9c, a PSD-95 inhibitor, is shown to reduce stroke-induced behavioural and neuroanatomical deficits in cynomolgous macaques when administered in the presence of an ischemic penumbra, suggesting the potential of PSD-95 inhibition as a neuroprotectant strategy for clinical investigation.

    • Douglas J. Cook
    • , Lucy Teves
    •  & Michael Tymianski

  • News & Views |

    Once a blood vessel supplying the brain has been blocked, the opportunity to prevent brain damage is fleeting. An alternative strategy might be to guide the damaged area onto the path to recovery. See Letter p.305

    • Kevin Staley

  • Letter |

    Following a stroke, there is generally limited functional recovery, but plasticity in adjacent intact areas may be critical to rehabilitation. These authors report that tonic GABAA inhibition is elevated in cortex immediately surrounding the stroke site. Furthermore, genetically or pharmacologically reducing tonic GABAA receptor signalling leads to improved functional and motor recovery in a mouse model of stroke, suggesting that this could be a new pharmacological target for stroke therapy.

    • Andrew N. Clarkson
    • , Ben S. Huang
    •  & S. Thomas Carmichael

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