中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (8): 1360-1361.doi: 10.4103/1673-5374.235238

• 观点:退行性病与再生 • 上一篇    下一篇

CHRNA7作为Arctic突变型β淀粉样蛋白的靶分子

  

  • 收稿日期:2018-05-31 出版日期:2018-08-15 发布日期:2018-08-15

Cholinergic receptor, nicotinic, alpha 7 as a target molecule of Arctic mutant amyloid β

Naoya Sawamura1, 2, Ye Ju1, Toru Asahi1, 2   

  1. 1 Faculty of Science and Engineering, Waseda University, Tokyo, Japan;
    2 Research Organization for Nano & Life Innovation, Waseda University, Tokyo, Japan
  • Received:2018-05-31 Online:2018-08-15 Published:2018-08-15
  • Contact: Naoya Sawamura, Ph.D.,naoya.sawamura@gmail.com or naoya@aoni.waseda.jp.
  • Supported by:

    This work was supported by a grant KAKENHI 15K06786 and the Center of Innovation Science and Technology based Radical Innovation and Entrepreneurship Program (COISTREAM) of the Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan.

摘要:

orcid: 0000-0003-4753-1119 (Naoya Sawamura)

Abstract:

Alzheimer’s disease (AD) is a progressive cognitive disorder that develops predominantly in elderly patients and is characterized by cognitive impairments affecting memory,learning, and attention. As the prevalence of AD is increasing concurrently with an increase in the aging demographic of society, the elucidation of its cause and underlying developmental mechanisms, as well as the development of preventive and therapeutic methods are eagerly awaited. Pathological features of AD include the appearance of senile plaques and neurofibrillary tangles throughout the cerebral cortex. Senile plaques appear to precede neurofibrillary tangles and are considered to be closely involved in the pathogenesis of AD. It is believed that the major constituent of senile plaques is amyloid β protein (Aβ), which then self-aggregates, forming the senile plaques.