Physical Exercise as an Effective Factor in Alzheimer Disease

  • سال انتشار: 1398
  • محل انتشار: سومین همایش بین المللی التهاب سیستم عصبی و سومین فستیوال دانشجویی علوم اعصاب
  • کد COI اختصاصی: NIMED03_292
  • زبان مقاله: انگلیسی
  • تعداد مشاهده: 411
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نویسندگان

Negar Khodaeinia

National Research Center of Genetic Engineering and Biotechnology (NIGEB), Department of Medical Genetics, Tehran, Iran

Zahra Farjami

Department of Modern Sciences and Technologies, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Amirhossein Ashnaei

Department of Modern Sciences and Technologies, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Neshat Ebrahimi

Laboratory of Cedars-Sinai Medical Center, Los Angles, California, USA

چکیده

disease (AD) is a progressive disease that destroys memory and other important mental activities. Scientists have found that remainingrelatively active can lead to better brain activities in those at risk of developing AD. In some Meta-analyses of prospective investigations, a significantly reduced risk of dementia related to midlife exercise have been proven. Most studies have been performed on animalmodels about the effects of exercise on brain β-amyloid deposition, showed that the level of amyloid plaques are reducing significantly. In another study about the serum BDNF levels and exercise have recognized major transient increases of circulating BDNF with shorttermaerobic exercise. This information recommend that aerobic exercise is related to a decreased risk of cognitive impairment and dementia. A convergence of data from both human and animal studies proposes that aerobic exercise may reduce development of neurodegenerative processes and age-association loss of synapses. Conclusion: This may occur by a direct effect on neurodegenerative disease procedures orsimplification of neuroprotective neurotrophic factors cognitive impairment and dementia. A convergence of data from both human and animal studies proposes that aerobic exercise may reduce development of neurodegenerative processes and age-association lossof synapses. Conclusion: This may occur by a direct effect on neurodegenerative disease procedures or simplification of neuroprotective neurotrophic factors

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