Neural Regeneration Research ›› 2018, Vol. 13 ›› Issue (8): 1360-1361.doi: 10.4103/1673-5374.235238

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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.

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.