中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (2): 261-262.doi: 10.4103/1673-5374.265553

• 观点:退行性病与再生 • 上一篇    下一篇

确定瑜伽逆转阿尔茨海默病症状的机制

  

  • 出版日期:2020-02-15 发布日期:2020-05-25

Determining the mechanism behind yoga’s effects on preventing the symptoms of Alzheimer’s disease

Adithy Hassan1, Meghan Robinson2, Stephanie M. Willerth1,3   

  1. 1Division of Medical Sciences, 3800 Finnerty Road, University of Victoria, Victoria, British Columbia, Canada  2The Vancouver Prostate Centre, Vancouver, British Columbia, Canada  3Department of Mechanical Engineering, University of Victoria, Victoria, British Columbia, Canada; Centre for Biomedical Research, University of Victoria, Victoria, British Columbia, Canada; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada 
  • Online:2020-02-15 Published:2020-05-25
  • Contact: Stephanie M. Willerth, PhD, willerth@uvic.ca.
  • Supported by:
    This work was provided by the Canada Research Chairs program and the NSERC Discovery Grants program (to SMW).

摘要: orcid: 0000-0002-1665-7723 (Stephanie M. Willerth)

Abstract: Dementia refers to a variety of conditions that affect the normal function of the brain, leading to symptoms like memory loss, issues with problem solving, difficulty in processing thoughts and disordered language (McKhann et al., 2011). AD serves as one of the major causes of dementia as it is responsible for ~80% of its cases according to the Alzheimer’s Association. AD affects the ability of neurons, the major information transmitting cells of both the peripheral and central nervous system, to send and receive signals through the body, leading to the aforementioned symptoms associated with dementia. The biological hallmarks of AD include the presence of amyloid beta (Aβ) plaques as well as neurofibrillary tangles containing a protein called tau (Lane et al., 2018). These proteins disrupt the normal function of neurons through a variety of mechanisms. In particular, AD first results in a loss of a specific neuronal subtype – the cholinergic neurons found in the basal forebrain - by reducing the expression levels of choline acetyltransferase. This enzyme breaks down acetylcholine, a neurotransmitter expressed in the neuromuscular junction, resulting in the loss of normal brain function. This loss of acetylcholine in AD patients was first noted in the late 1970s, and is now known to correlate with reduced cortical choline acetyltransferase, the enzyme responsible for synthesizing acetycholine from choline, which in turn correlates with neuritic plaque numbers and reduced Mini-Mental State Exam scores (Gauthier, 2002). Currently available pharmacological treatments for AD focus on inhibiting the loss of choline acetyltransferase, but do not represent a longterm cure.