中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (2): 315-316.doi: 10.4103/1673-5374.343905

• 观点:退行性病与再生 • 上一篇    下一篇

CHMP2B 额颞叶痴呆的突触病变突出突触小泡周期作为治疗靶点

  

  • 出版日期:2023-02-15 发布日期:2022-08-06

Synaptopathy in CHMP2B frontotemporal dementia highlights the synaptic vesicle cycle as a therapeutic target

Miranda Robbins, Emma L. Clayton*   

  1. MRC Laboratory of Molecular Biology; Department of Zoology, University of Cambridge, Cambridge, UK (Robbins M)
    UK Dementia Research Institute at King’s College London; Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, Maurice Wohl Clinical Neuroscience Institute, London, UK (Clayton EL)
  • Online:2023-02-15 Published:2022-08-06
  • Contact: Emma L. Clayton, PhD, emma.clayton@kcl.ac.uk.
  • Supported by:
    MR was funded by MRC LMB. EC acknowledges funding from Alzheimer’s Research UK (PPG2018B-017) and the UK Dementia Research Institute which receives its funding from DRI Ltd., funded by the UK Medical Research Council, Alzheimer’s Society, and Alzheimer’s Research UK.

摘要: https://orcid.org/0000-0003-0937-2874 (Emma L. Clayton)

Abstract: Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are both devastating neurodegenerative conditions. Despite affecting different regions of the nervous system (FTD affecting primarily the frontal and temporal lobes, whilst ALS presents with motor neuron loss), there is significant overlap between these conditions in terms of genetics, pathology, and disease mechanisms, and they are therefore often grouped as a spectrum of symptoms under the heading FTD/ALS (Abramzon et al., 2020). Significantly, there is currently no cure for ALS or FTD. However, recent mechanistic insight points to a novel pathway to target for potential therapeutic intervention.