Parkinson's disease articles within Nature

Featured

  • Article |

    Monoamines and neurotoxicants share a binding pocket in VMAT1 featuring polar sites for specificity and a wrist-and-fist shape for versatility, and monoamine enrichment in storage vesicles arises from dominant import via favoured lumenal-open transition of VMAT1 and protonation-precluded binding during its cytoplasmic-open transition.

    • Jin Ye
    • , Huaping Chen
    •  & Weikai Li

  • Article |

    The authors report on the structures of α-synuclein filaments from the brains of individuals with Parkinson's disease, Parkinson's disease dementia and dementia with Lewy bodies and how they differ from those seen in multiple system atrophy.

    • Yang Yang
    • , Yang Shi
    •  & Michel Goedert

  • Research Briefing |

    Parkinson’s disease causes slowness of movement, tremor and stiffness, along with mood symptoms such as depression. The brain’s parafascicular thalamus is shown to contain distinct neural circuits for locomotion, motor learning and depression-like states, and targeting these circuits alleviates some deficits in a mouse model of the disease.

  • News & Views |

    Mice in which organelles called mitochondria are disrupted in vulnerable neuronal cells provide a new model of Parkinson’s disease. The pattern of neurodegeneration challenges long-held ideas about the disease’s motor symptoms.

    • Zak Doric
    •  & Ken Nakamura

  • News & Views |

    Grafts of stem-cell-derived precursors of dopamine neurons could be used to treat Parkinson’s disease, but this approach has limitations. Injecting a growth factor three weeks after transplantation can overcome some of these limits.

    • Lorenz Studer
    •  & Viviane Tabar

  • Article |

    The lysosomal polyamine transporter ATP13A2 controls the cellular polyamine content, and impaired lysosomal polyamine export represents a lysosome-dependent cell death pathway that may be implicated in ATP13A2-associated neurodegeneration.

    • Sarah van Veen
    • , Shaun Martin
    •  & Peter Vangheluwe

  • News & Views |

    PINK1 and parkin proteins help to degrade damaged mitochondrial organelles, and abnormalities in these proteins are linked to Parkinson’s disease. Mouse studies reveal that the proteins act to prevent inflammation.

    • Alexandra Stolz
    •  & Ivan Dikic

  • News & Views |

    Conventional models propose that activity levels in two neuronal pathways, which have opposing effects on movement, become imbalanced in Parkinson’s disease. Analyses in mice point to a more complex reality.

    • Thomas Wichmann

  • News & Views |

    Structures of an unusual enzymatic domain in PINK1 provide insights into how this protein regulates the function of organelles called mitochondria, and how mutations in PINK1 contribute to Parkinson’s disease.

    • Salima Daou
    •  & Frank Sicheri

  • 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 |

    Deep brain stimulation is a proven treatment for Parkinson's disease. The only thing left to find out is how it works.

    • Michael Eisenstein

  • Outlook |

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

    • Lauren Gravitz

  • Outlook |

    In the 200 years since Parkinson's disease was first described, the understanding and management of the disease has come a long way. But researchers have yet to unlock all of its secrets. By Liam Drew.

    • Liam Drew

  • Outlook |

    Biomarkers will be essential if research on Parkinson's is to progress, but their discovery depends on scientists sharing data, says Mark Frasier.

    • Mark Frasier

  • 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

  • Outlook |

    Two competing hypotheses about Parkinson's and Gaucher's diseases need to be knitted together, say Anthony H. Futerman and John Hardy.

    • Anthony H. Futerman
    •  & John Hardy

  • News & Views |

    Certain sequence variants of the α-synuclein gene are linked to the risk of Parkinson's disease. An analysis of these variants using gene-editing technology provides a possible explanation for this increased risk. See Letter p.95

    • Asa Abeliovich
    •  & Herve Rhinn

  • News & Views |

    The native structure of the protein α-synuclein, which is implicated in Parkinson's disease, is controversial. In-cell nuclear magnetic resonance now shows that it remains disordered when loaded into living cells. See Article p.45

    • T. Reid Alderson
    •  & Ad Bax

  • 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

  • Article |

    A short segment of α-synuclein called NACore (residues 68–78) is responsible for the formation of amyloid aggregates responsible for cytotoxicity in Parkinson disease; here the nanocrystal structure of this invisible-to-optical-microscopy segment is determined using micro-electron diffraction, offering insight into its function and simultaneously demonstrating the first use of micro-electron diffraction to solve a previously unknown protein structure.

    • Jose A. Rodriguez
    • , Magdalena I. Ivanova
    •  & David S. Eisenberg

  • Article |

    Damaged mitochondria are removed by mitophagy, and defects in mitophagy are linked to Parkinson’s disease; here it is shown that USP30, a deubiquitinase localized to mitochondria, antagonizes mitophagy by removing the ubiquitin tags put in place by Parkin, USP30 inhibition is therefore potentially beneficial for Parkinson’s disease by promoting mitochondrial clearance and quality control.

    • Baris Bingol
    • , Joy S. Tea
    •  & Morgan Sheng

  • Letter |

    Ubiquitin, known for its role in post-translational modification of other proteins, undergoes post-translational modification itself; after a decrease in mitochondrial membrane potential, the kinase enzyme PINK1 phosphorylates ubiquitin at Ser 65, and the phosphorylated ubiquitin then interacts with ubiquitin ligase (E3) enzyme parkin, which is also phosphorylated by PINK1, and this process is sufficient for full activation of parkin enzymatic activity.

    • Fumika Koyano
    • , Kei Okatsu
    •  & Noriyuki Matsuda

  • Outlook |

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

    • Moheb Costandi

  • Letter |

    Analysis of the respective crystal structures of the yeast single-component type-II NADH dehydrogenase Ndi1 in its substrate-free form and when bound to NADH, ubiquinone and NADH–ubiquinone shows that Ndi1 homodimerization through its carboxy-terminal domain is critical for its catalytic activity and membrane targeting.

    • Yue Feng
    • , Wenfei Li
    •  & Maojun Yang

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