S-adenosylmethionine Administration Attenuates Low Brain-Derived Neurotrophic Factor Expression Induced by Chronic Cerebrovascular Hypoperfusion or Beta Amyloid Treatment

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• 作者：Qian Li ; Jing Cui ; Chen Fang ; Xiaowen Zhang ; Liang Li
• 关键词：Cerebrovascular hypoperfusion ; Beta amyloid ; Brain ; derived neurotrophic factor ; S ; adenosylmethionine
• 刊名：Neuroscience Bulletin
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：32
• 期：2
• 页码：153-161
• 全文大小：1,146 KB
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• 作者单位：Qian Li (1)
  Jing Cui (1)
  Chen Fang (1)
  Xiaowen Zhang (1)
  Liang Li (1)
  
  1. Department of Pathology, Capital Medical University, Beijing, 100069, China
  
• 刊物主题：Neurosciences; Human Physiology; Anesthesiology; Anatomy; Neurology; Pain Medicine;
• 出版者：Springer Berlin Heidelberg
• ISSN：1995-8218

文摘

Chronic cerebrovascular hypoperfusion is a high-risk factor for Alzheimer’s disease (AD) as it is conducive to beta amyloid (Aβ) over-production. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family widely expressed in the central nervous system. The structure of the rat BDNF gene is complex, consisting of eight non-coding exons (I–VIII) and one coding exon (IX). The BDNF gene is transcribed from multiple promoters located upstream of different 5′ non-coding exons to produce a heterogeneous population of BDNF mRNAs. S-adenosylmethionine (SAM) produced in the methionine cycle is the primary methyl donor and the precursor of glutathione. In this study, a cerebrovascular hypoperfusion rat model and an Aβ intrahippocampal injection rat model were used to explore the expression profiles of all BDNF transcripts in the hippocampus with chronic cerebrovascular hypoperfusion or Aβ injection as well as with SAM treatment. We found that the BDNF mRNAs and protein were down-regulated in the hippocampus undergoing chronic cerebrovascular hypoperfusion as well as Aβ treatment, and BDNF exons IV and VI played key roles. SAM improved the low BDNF expression following these insults mainly through exons IV and VI. These results suggest that SAM plays a neuroprotective role by increasing the expression of endogenous BDNF and could be a potential target for AD therapy.