Neurological disorders articles within Nature

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  • Outlook |

    As the development of treatments for Alzheimer’s disease continues to stumble, is it time for researchers to broaden their list of the condition’s potential causes?

    • Simon Makin

  • Outlook |

    Despite gaps in our understanding of the biology that underlies this neurodegenerative condition, potential treatments are on the horizon.

    • Herb Brody

  • Outlook |

    Although it usually affects people in middle age, the inherited neurodegenerative condition can also develop in children and teenagers.

    • Elie Dolgin

  • Outlook |

    Although potential treatments are now entering the pipeline, the molecular cause and progression of Huntington’s disease continue to elude researchers.

    • Anna Nowogrodzki

  • News & Views |

    The brain’s resident immune cells retain a long-lasting memory of peripheral inflammation. This memory can influence the response to stroke and the progression of Alzheimer’s disease in mouse models.

    • Alexi Nott
    •  & Christopher K. Glass

  • News & Views |

    Low-complexity protein aggregates are a hallmark of neurodegeneration. High-resolution snapshots of the structure of one such aggregate offer an unprecedented view of how these proteins disrupt crucial cellular functions.

    • Laura Pontano Vaites
    •  & J. Wade Harper

  • Letter |

    The structure of huntingtin in complex with an interactor is determined to an overall resolution of 4 Å, paving the way for improved understanding of the cellular functions of this protein.

    • Qiang Guo
    • , Bin Huang
    •  & Stefan Kochanek

  • Letter |

    Experimental evidence that global Kctd13 reduction leads to increased RhoA levels that reduce synaptic transmission, implicating RhoA as a potential therapeutic target for neuropsychiatric disorders associated with copy-number variants that include KCTD13.

    • Christine Ochoa Escamilla
    • , Irina Filonova
    •  & Craig M. Powell

  • Outlook |

    Let's start describing ALS on the basis of its cause, not on whether someone obtained a relevant family history, says Ammar Al-Chalabi.

    • Ammar Al-Chalabi

  • Outlook |

    Research ranging in scale from cells to populations is rapidly closing in on what goes awry in the body in 'non-familial' ALS, and what environmental factors might contribute.

    • Carolyn Brown

  • Outlook |

    Machine learning might identify patients earlier, predict their outcomes better, and assign them more efficiently to appropriate clinical trials.

    • Neil Savage

  • Outlook |

    For years, researchers missed the most common genetic cause of ALS. Now they're on an accelerated track to treat it.

    • Elie Dolgin

  • News & Views |

    Mutations in embryonic blood-cell precursors called erythro-myeloid progenitors cause abnormal activation of their descendants — immune cells called microglia — leading to neurodegeneration in mice. See Letter p.389

    • Stefan P. Tarnawsky
    •  & Mervin C. Yoder

  • Editorial |

    Sports organizations are only starting to understand the harm that can be inflicted by high-contact activities. Science must play its part in highlighting the problem and in aiding diagnosis.

  • News & Views |

    The protein tau forms abnormal filamentous aggregates called tangles in the brains of people with neurodegeneration. Structures of two such filaments offer pathways to a deeper understanding of Alzheimer's disease. See Article p.185

    • David S. Eisenberg
    •  & Michael R. Sawaya

  • News & Views |

    Droplet-like assemblies of RNA in cell nuclei are associated with certain neurodegenerative diseases. Experiments reveal that these assemblies become 'frozen' gels in cells, potentially explaining their toxicity. See Article p.243

    • David W. Sanders
    •  & Clifford P. Brangwynne

  • News & Views |

    Mutant proteins that contain stretches called polyQ repeats can misfold or form aggregates linked to neurodegeneration. It emerges that some polyQ-containing proteins regulate a process that degrades misfolded proteins. See Letter p.108

    • Dale D. O. Martin
    •  & Michael R. Hayden

  • Letter |

    The polyglutamine domain in ataxin 3, which is expanded in spinocerebellar ataxia type 3, allows normal ataxin 3 to interact with and deubiquitinate beclin 1 and thereby to promote autophagy.

    • Avraham Ashkenazi
    • , Carla F. Bento
    •  & David C. Rubinsztein

  • News & Views |

    Bacterial residents of the human body often provide beneficial effects, but some can be harmful. The action of gut bacteria has been found to be tightly linked to neurodegeneration in a mouse model of Parkinson's disease.

    • Daniel Erny
    •  & Marco Prinz

  • News & Views |

    Molecules that inhibit the synthesis of the ataxin 2 protein can ameliorate the effects of two neurodegenerative diseases in mouse models, raising hopes for the success of this approach in clinical trials. See Letters p.362 & p.367

    • Ke Zhang
    •  & Jeffrey D. Rothstein

  • Article |

    Whole-exome analysis of individuals with developmental disorders shows that de novo mutations can equally cause loss or altered protein function, but that most mutations causing altered protein function have not yet been described.

    • Jeremy F. McRae
    • , Stephen Clayton
    •  & Matthew E. Hurles

  • Letter |

    Structural differences in 40- and 42-residue-long amyloid-β fibrils seeded in vitro from the cortical tissue of patients with different clinical subtypes of Alzheimer’s disease suggest that different fibril structures form in different disease variants and with different peptide lengths.

    • Wei Qiang
    • , Wai-Ming Yau
    •  & Robert Tycko

  • News & Views |

    Identification of a previously uncharacterized genetic disease highlights DNA repair as a shared mechanism in neurodegenerative disorders, and suggests potential therapeutic approaches to tackling them. See Letter p.87

    • Christopher A. Ross
    •  & Ray Truant

  • News & Views |

    Electrical oscillations generated by neural circuits are disrupted in Alzheimer's disease. Restoring these oscillations in mouse models activates immune cells to clear disease-associated amyloid-β protein from the brain. See Article p.230

    • Liviu Aron
    •  & Bruce A. Yankner

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