Neurological disorders articles within Nature

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  • News & Views |

    Retinal-cell transplants restore vision in mouse models of retinal degeneration. It emerges that the transplant leads to an exchange of material between donor and host cells — not to donor-cell integration into the retina, as had been presumed.

    • Michael A. Dyer

  • News Feature |

    Three things are needed to turn the tide on the costliest crisis in health care.

    • Elie Dolgin

  • Outlook |

    The characteristic brain pathology and motor symptoms of Parkinson's disease are well established. But the details of the disease's cause and course are much murkier.

    • Sarah Deweerdt

  • Outlook |

    By bootstrapping existing technologies, researchers can gain a minute-by-minute understanding of a patient's disease.

    • Lauren Gravitz

  • Outlook |

    Non-motor symptoms such as sleep disorders and a poor sense of smell may hold the key to diagnosing Parkinson's disease before the characteristic tremor starts.

    • Katherine Bourzac

  • Outlook |

    A controversial theory that could revolutionize our understanding of Parkinson's disease is gaining ground. But not everybody is convinced that misfolded proteins that spread in the brain are the cause of the disease.

    • Simon Makin

  • Article |

    Aducanumab, a human monoclonal antibody that selectively targets aggregated Aβ, reduces soluble and insoluble Aβ in the brain, an action accompanied by a dose-dependent slowing of clinical decline in treated patients.

    • Jeff Sevigny
    • , Ping Chiao
    •  & Alfred Sandrock

  • Letter |

    A human neurodevelopmental model fills the current knowledge gap in the cellular biology of Williams syndrome and could lead to further insights into the molecular mechanism underlying the disorder and the human social brain.

    • Thanathom Chailangkarn
    • , Cleber A. Trujillo
    •  & Alysson R. Muotri

  • Brief Communications Arising |

    • John Collinge
    • , Zane Jaunmuktane
    •  & Sebastian Brandner

  • Article |

    Sustained delivery of axon-specific growth factors not typically present in spinal cord lesions allows for robust axonal regrowth only if the astrocytic scar is present—a result that questions the prevailing dogma and suggests that astrocytic scarring aids rather than prevents central nervous system axon regeneration post injury.

    • Mark A. Anderson
    • , Joshua E. Burda
    •  & Michael V. Sofroniew

  • Outlook |

    Future generations may have less to fear from cognitive decline thanks to microscopic insights into the ageing brain, and interventions from unexpected quarters.

    • Annabel McGilvray

  • News & Views |

    A molecular cascade involving the transcription factor SIX6 and its target gene p16INK4a causes the death of neurons that link the eye to the brain. This discovery deepens our understanding of a common form of blindness, glaucoma.

    • Andrew D. Huberman
    •  & Rana N. El-Danaf

  • Letter |

    Deep brain stimulation (DBS) of the fimbria–fornix—a region that provides input to the hippocampus—is shown to restore hippocampus-dependent memory and hippocampal long-term potentiation and neurogenesis in a mouse model of Rett syndrome, suggesting that DBS, which is already used in the treatment of several neurological conditions, could be a viable approach to mitigating cognitive impairment in Rett syndrome and other disorders of childhood intellectual disability.

    • Shuang Hao
    • , Bin Tang
    •  & Jianrong Tang

  • News & Views |

    People who died of the neurodegenerative condition Creutzfeldt-Jakob disease after treatment with cadaver-derived human growth hormone also developed some of the pathological traits of Alzheimer's disease. See Letter p.247

    • Mathias Jucker
    •  & Lary C. Walker

  • News & Views |

    An ultra-high-resolution structure of the core segment of assembled α-synuclein — the protein that aggregates in the brains of patients with Parkinson's disease — has been determined. A neurobiologist and a structural biologist discuss the implications of this advance. See Article p.486

    • Michel Goedert
    •  & Yifan Cheng

  • Letter |

    Treatment of children with human cadaver-derived growth hormone (c-hGH) contaminated with prions resulted in transmission of Creutzfeldt–Jakob disease (CJD); unexpectedly, in an autopsy study of eight such iCJD patients, the authors found amyloid-β deposition in the grey matter typical of that seen in Alzheimer's disease and amyloid-β in the blood vessel walls characteristic of cerebral amyloid angiopathy, consistent with iatrogenic transmission of amyloid-β pathology in addition to CJD and suggests that healthy c-hGH-exposed individuals may also be at risk of Alzheimer's disease and cerebral amyloid angiopathy.

    • Zane Jaunmuktane
    • , Simon Mead
    •  & Sebastian Brandner

  • News & Views |

    Expansion of a repetitive DNA sequence is associated with neurodegeneration. Three studies identify genes involved in nuclear import and export that can mediate the toxicity this expansion causes. See Article p.56 & Letter p.129

    • Bennett W. Fox
    •  & Randal S. Tibbetts

  • Letter |

    An unbiased genetic screen in Drosophila expressing G4C2-repeat-containing transcripts (repeats that in human cause pathogenesis in C9orf72-related neurological disease) finds genes that encode components of the nuclear pore and nucleocytoplasmic transport machinery, and reveals that G4C2 expanded-repeat-induced alterations in nucleocytoplasmic transport contribute to C9orf72 pathology and neurodegeneration.

    • Brian D. Freibaum
    • , Yubing Lu
    •  & J. Paul Taylor

  • News & Views |

    Aggregates of α-synuclein protein can form in various cell types and cause different neurodegenerative disorders. The existence of strains with distinct structural conformations might explain this variability. See Letter p.340

    • Seung-Jae Lee
    •  & Eliezer Masliah

  • News & Views |

    A genetic variant of PrP, the protein that forms prions, confers protection against the human prion disease kuru by inhibiting the conversion of functional isoforms to the abnormal, disease-causing conformation. See Letter p.478

    • Glenn Telling

  • Letter |

    Whole-exome sequencing reveals that a rare variant of phospholipase D3 (PLD3(V232M)) segregates with Alzheimer’s disease status in two independent families and doubles risk for the disease in case–control series, and that several other PLD3 variants increase risk for Alzheimer’s disease in African Americans and people of European descent.

    • Carlos Cruchaga
    • , Celeste M. Karch
    •  & Alison M. Goate

  • Article |

    This study reports a global analysis of binding sites for over 200 RNA-binding proteins (RBPs) from 24 species; conserved RNA-binding motifs are identified, and their analysis allows prediction of interaction sites based on the sequence of the RNA-binding domain alone.

    • Debashish Ray
    • , Hilal Kazan
    •  & Timothy R. Hughes

  • Outlook |

    Sleep disturbances may be an early sign of neurodegenerative diseases — but could sleep deficits cause these conditions in the first place?

    • Moheb Costandi

  • Outlook |

    A combination of drugs and cognitive behavioural therapy may finally put an end to the misery of sleepless nights.

    • James Mitchell Crow

  • Article |

    Presenilin, the catalytic component of γ-secretase, cleaves amyloid precursor protein into short peptides that form the plaques that are found in the brains of patients with Alzheimer’s disease; here the structure of a presenilin homologue is described, which will serve as a framework for understanding the mechanisms of action of presenilin and γ-secretase.

    • Xiaochun Li
    • , Shangyu Dang
    •  & Yigong Shi

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