PMID- 26983613
OWN - NLM
STAT- MEDLINE
DCOM- 20161228
LR  - 20181113
IS  - 1995-8218 (Electronic)
IS  - 1673-7067 (Print)
IS  - 1995-8218 (Linking)
VI  - 32
IP  - 2
DP  - 2016 Apr
TI  - S-adenosylmethionine Administration Attenuates Low Brain-Derived Neurotrophic 
      Factor Expression Induced by Chronic Cerebrovascular Hypoperfusion or Beta 
      Amyloid Treatment.
PG  - 153-61
LID - 10.1007/s12264-016-0023-z [doi]
AB  - Chronic cerebrovascular hypoperfusion is a high-risk factor for Alzheimer's 
      disease (AD) as it is conducive to beta amyloid (Abeta) 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 Abeta intrahippocampal injection rat model were used 
      to explore the expression profiles of all BDNF transcripts in the hippocampus 
      with chronic cerebrovascular hypoperfusion or Abeta 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 Abeta 
      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.
FAU - Li, Qian
AU  - Li Q
AD  - Department of Pathology, Capital Medical University, Beijing, 100069, China.
FAU - Cui, Jing
AU  - Cui J
AD  - Department of Pathology, Capital Medical University, Beijing, 100069, China.
FAU - Fang, Chen
AU  - Fang C
AD  - Department of Pathology, Capital Medical University, Beijing, 100069, China.
FAU - Zhang, Xiaowen
AU  - Zhang X
AD  - Department of Pathology, Capital Medical University, Beijing, 100069, China.
FAU - Li, Liang
AU  - Li L
AD  - Department of Pathology, Capital Medical University, Beijing, 100069, China. 
      liliang8698@yeah.net.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160316
PL  - Singapore
TA  - Neurosci Bull
JT  - Neuroscience bulletin
JID - 101256850
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Peptide Fragments)
RN  - 0 (RNA, Messenger)
RN  - 0 (amyloid beta-protein (1-42))
RN  - 7LP2MPO46S (S-Adenosylmethionine)
SB  - IM
MH  - Amyloid beta-Peptides/*toxicity
MH  - Analysis of Variance
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - *Carotid Stenosis/drug therapy/metabolism/pathology
MH  - Disease Models, Animal
MH  - Exons/drug effects/physiology
MH  - Gene Expression Regulation/*drug effects
MH  - Hippocampus/drug effects/metabolism
MH  - Male
MH  - Neuroprotective Agents/*therapeutic use
MH  - Peptide Fragments/*toxicity
MH  - RNA, Messenger
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - S-Adenosylmethionine/*therapeutic use
MH  - Time Factors
PMC - PMC5563744
OTO - NOTNLM
OT  - Beta amyloid
OT  - Brain-derived neurotrophic factor
OT  - Cerebrovascular hypoperfusion
OT  - S-adenosylmethionine
EDAT- 2016/03/18 06:00
MHDA- 2016/12/29 06:00
PMCR- 2017/04/01
CRDT- 2016/03/18 06:00
PHST- 2015/09/28 00:00 [received]
PHST- 2015/12/14 00:00 [accepted]
PHST- 2016/03/18 06:00 [entrez]
PHST- 2016/03/18 06:00 [pubmed]
PHST- 2016/12/29 06:00 [medline]
PHST- 2017/04/01 00:00 [pmc-release]
AID - 10.1007/s12264-016-0023-z [pii]
AID - 23 [pii]
AID - 10.1007/s12264-016-0023-z [doi]
PST - ppublish
SO  - Neurosci Bull. 2016 Apr;32(2):153-61. doi: 10.1007/s12264-016-0023-z. Epub 2016 
      Mar 16.