中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (2): 335-336.doi: 10.4103/1673-5374.346477

• 观点:退行性病与再生 • 上一篇    下一篇

微管亲和调节激酶 (MARK/Par1) 亚型差异调节阿尔茨海默病样 TAU 错配和 Aβ 介导的突触病理学

  

  • 出版日期:2023-02-15 发布日期:2022-08-06

Microtubule affinity regulating kinase (MARK/Par1) isoforms differentially regulate Alzheimer-like TAU missorting and Aβ-mediated synapse pathology

Jana Chudobová, Hans Zempel*   

  1. Institute of Human Genetics, Faculty of Medicine and University Hospital Cologne; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany
  • Online:2023-02-15 Published:2022-08-06
  • Contact: Hans Zempel, PhD, MD, MSc, hans.zempel@uk-koeln.de.
  • Supported by:
    This work was supported by the Koeln Fortune Program/Faculty of Medicine, University of Cologne, and the Else-Kröner-Fresenius-Stiftung.

摘要: https://orcid.org/0000-0002-7510-3077 (Hans Zempel)

Abstract: Importance of TAU protein for dementia syndromes: Dementia currently affects about 55 million people worldwide, with Alzheimer´s disease (AD) being the most prevalent form. The one crucial pathological hallmark of AD that correlates best with loss of synapses and cognitive decline are the so-called intracellular neurofibrillary tangles composed of mislocalized/missorted and hyperphosphorylated TAU protein (Naseri et al., 2019). Many other neurodegenerative diseases, both genetic and non-genetic, are characterized by neurofibrillary tangles or pathological accumulation of the protein TAU and are thus termed “tauopathies”. Tauopathies include AD and related aging-associated dementia syndromes like frontotemporal dementia and variants thereof (progressive supranuclear palsy, Pick‘s disease, corticobasal degeneration), but also childhood-onset genetic diseases (Zimmer-Bensch and Zempel, 2021).