S-adenosylmethionine Administration Attenuates Low Brain-Derived Neurotrophic Factor Expression Induced by Chronic Cerebrovascular Hypoperfusion or Beta Amyloid Treatment
Chronic cerebrovascular hypoperfusion is a high-risk factor for Alzheimer＇s disease（AD） as it is conducive to beta amyloid（Ab） over-production. Brainderived neurotrophic factor（BDNF） is a member of the neurotrophin family widely expressed in the central nervous system. The structure of the rat BDNF...
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| Veröffentlicht in: | Neuroscience bulletin 2016-04, Vol.32 (2), p.153-161 |
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| creator | Li, Qian Cui, Jing Fang, Chen Zhang, Xiaowen Li, Liang |
| description | Chronic cerebrovascular hypoperfusion is a high-risk factor for Alzheimer＇s disease（AD） as it is conducive to beta amyloid（Ab） over-production. Brainderived 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 50 noncoding exons to produce a heterogeneous population of BDNF m RNAs. 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 Ab intrahippocampal injection rat model were used to explore the expression profiles of all BDNF transcripts in the hippocampus with chronic cerebrovascular hypoperfusion or Ab injection as well as with SAM treatment. We found that the BDNF m RNAs and protein were down-regulated in the hippocampus undergoing chronic cerebrovascular hypoperfusion as well as Ab 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. |
| doi_str_mv | 10.1007/s12264-016-0023-z |
| format | Article |
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Brainderived 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 50 noncoding exons to produce a heterogeneous population of BDNF m RNAs. 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 Ab intrahippocampal injection rat model were used to explore the expression profiles of all BDNF transcripts in the hippocampus with chronic cerebrovascular hypoperfusion or Ab injection as well as with SAM treatment. We found that the BDNF m RNAs and protein were down-regulated in the hippocampus undergoing chronic cerebrovascular hypoperfusion as well as Ab 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.</description><identifier>ISSN: 1673-7067</identifier><identifier>EISSN: 1995-8218</identifier><identifier>DOI: 10.1007/s12264-016-0023-z</identifier><identifier>PMID: 26983613</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Advertising executives ; Alzheimer's disease ; Amyloid beta-Peptides - toxicity ; Analysis of Variance ; Anatomy ; Anesthesiology ; Animals ; BDNF基因 ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Brain-Derived Neurotrophic Factor - genetics ; Brain-Derived Neurotrophic Factor - metabolism ; Carotid Stenosis - drug therapy ; Carotid Stenosis - metabolism ; Carotid Stenosis - pathology ; Disease Models, Animal ; Exons - drug effects ; Exons - physiology ; Gene Expression Regulation - drug effects ; Hippocampus - drug effects ; Hippocampus - metabolism ; Human Physiology ; Male ; Neurology ; Neuroprotective Agents - therapeutic use ; Neurosciences ; Original ; Original Article ; Pain Medicine ; Peptide Fragments - toxicity ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger ; S-adenosylmethionine ; S-Adenosylmethionine - therapeutic use ; S-腺苷甲硫氨酸 ; Target marketing ; Time Factors ; β-淀粉样蛋白 ; 大鼠模型 ; 慢性 ; 脑源性神经营养因子 ; 脑缺血 ; 诱导</subject><ispartof>Neuroscience bulletin, 2016-04, Vol.32 (2), p.153-161</ispartof><rights>Shanghai Institutes for Biological Sciences, CAS and Springer Science+Business Media Singapore 2016</rights><rights>COPYRIGHT 2016 Springer</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c536t-a9ee532cce5711131c07ef8d7edca57bb8c2f7d7df273b2f0877c928414ecc2c3</citedby><cites>FETCH-LOGICAL-c536t-a9ee532cce5711131c07ef8d7edca57bb8c2f7d7df273b2f0877c928414ecc2c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/91222B/91222B.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5563744/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5563744/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26983613$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Cui, Jing</creatorcontrib><creatorcontrib>Fang, Chen</creatorcontrib><creatorcontrib>Zhang, Xiaowen</creatorcontrib><creatorcontrib>Li, Liang</creatorcontrib><title>S-adenosylmethionine Administration Attenuates Low Brain-Derived Neurotrophic Factor Expression Induced by Chronic Cerebrovascular Hypoperfusion or Beta Amyloid Treatment</title><title>Neuroscience bulletin</title><addtitle>Neurosci. Bull</addtitle><addtitle>Neuroscience Bulletin</addtitle><description>Chronic cerebrovascular hypoperfusion is a high-risk factor for Alzheimer＇s disease（AD） as it is conducive to beta amyloid（Ab） over-production. Brainderived 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 50 noncoding exons to produce a heterogeneous population of BDNF m RNAs. 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 Ab intrahippocampal injection rat model were used to explore the expression profiles of all BDNF transcripts in the hippocampus with chronic cerebrovascular hypoperfusion or Ab injection as well as with SAM treatment. We found that the BDNF m RNAs and protein were down-regulated in the hippocampus undergoing chronic cerebrovascular hypoperfusion as well as Ab 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.</description><subject>Advertising executives</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - toxicity</subject><subject>Analysis of Variance</subject><subject>Anatomy</subject><subject>Anesthesiology</subject><subject>Animals</subject><subject>BDNF基因</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Brain-Derived Neurotrophic Factor - genetics</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Carotid Stenosis - drug therapy</subject><subject>Carotid Stenosis - metabolism</subject><subject>Carotid Stenosis - pathology</subject><subject>Disease Models, Animal</subject><subject>Exons - drug effects</subject><subject>Exons - physiology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Human Physiology</subject><subject>Male</subject><subject>Neurology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Neurosciences</subject><subject>Original</subject><subject>Original Article</subject><subject>Pain Medicine</subject><subject>Peptide Fragments - toxicity</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger</subject><subject>S-adenosylmethionine</subject><subject>S-Adenosylmethionine - therapeutic use</subject><subject>S-腺苷甲硫氨酸</subject><subject>Target marketing</subject><subject>Time Factors</subject><subject>β-淀粉样蛋白</subject><subject>大鼠模型</subject><subject>慢性</subject><subject>脑源性神经营养因子</subject><subject>脑缺血</subject><subject>诱导</subject><issn>1673-7067</issn><issn>1995-8218</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kk9v0zAYxiMEYqPwAbggi124ZPhPYicXpK5sbFIFB8bZcpw3rafEzmyn0H0kPiUuLRWTEPLBlt_n9_i1_WTZa4LPCcbifSCU8iLHhOcYU5Y_PMlOSV2XeUVJ9TStuWC5wFycZC9CuMOYY8GK59kJ5XXFOGGn2c-vuWrBurDtB4hr46yxgObtYKwJ0auYdtA8RrCTihDQ0n1HF14Zm38EbzbQos8weRe9G9dGoyulo_Po8sfoIYQde2PbSSdZs0WLtU_2Gi3AQ-PdRgU99cqj6-3oRvDd9BtI-AVEhebDtnemRbceVBzAxpfZs071AV4d5ln27erydnGdL798ulnMl7kuGY-5qgFKRrWGUhBCGNFYQFe1AlqtStE0laadaEXbUcEa2uFKCF3TqiAFaE01m2Uf9r7j1AwJSkd71cvRm0H5rXTKyMcVa9Zy5TayLDkTRZEM3h0MvLufIEQ5mKCh75UFNwVJhKiLgtJ0_iw720tXqgdpbJdeUumdXM4FETUtKWNJdf4PVRotDEY7C51J-48Asge0dyF46I7dEyx30ZH76MgUHbmLjnxIzJu_r30k_mQlCeheEFLJrsDLOzd5m77iv65vD52snV3dJ-5ozHlVlkIQyn4Bej3gIg</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Li, Qian</creator><creator>Cui, Jing</creator><creator>Fang, Chen</creator><creator>Zhang, Xiaowen</creator><creator>Li, Liang</creator><general>Springer Singapore</general><general>Springer</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160401</creationdate><title>S-adenosylmethionine Administration Attenuates Low Brain-Derived Neurotrophic Factor Expression Induced by Chronic Cerebrovascular Hypoperfusion or Beta Amyloid Treatment</title><author>Li, Qian ; Cui, Jing ; Fang, Chen ; Zhang, Xiaowen ; Li, Liang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c536t-a9ee532cce5711131c07ef8d7edca57bb8c2f7d7df273b2f0877c928414ecc2c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Advertising executives</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - toxicity</topic><topic>Analysis of Variance</topic><topic>Anatomy</topic><topic>Anesthesiology</topic><topic>Animals</topic><topic>BDNF基因</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Brain-Derived Neurotrophic Factor - genetics</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Carotid Stenosis - drug therapy</topic><topic>Carotid Stenosis - metabolism</topic><topic>Carotid Stenosis - pathology</topic><topic>Disease Models, Animal</topic><topic>Exons - drug effects</topic><topic>Exons - physiology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Human Physiology</topic><topic>Male</topic><topic>Neurology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Neurosciences</topic><topic>Original</topic><topic>Original Article</topic><topic>Pain Medicine</topic><topic>Peptide Fragments - toxicity</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger</topic><topic>S-adenosylmethionine</topic><topic>S-Adenosylmethionine - therapeutic use</topic><topic>S-腺苷甲硫氨酸</topic><topic>Target marketing</topic><topic>Time Factors</topic><topic>β-淀粉样蛋白</topic><topic>大鼠模型</topic><topic>慢性</topic><topic>脑源性神经营养因子</topic><topic>脑缺血</topic><topic>诱导</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Cui, Jing</creatorcontrib><creatorcontrib>Fang, Chen</creatorcontrib><creatorcontrib>Zhang, Xiaowen</creatorcontrib><creatorcontrib>Li, Liang</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuroscience bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Qian</au><au>Cui, Jing</au><au>Fang, Chen</au><au>Zhang, Xiaowen</au><au>Li, Liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>S-adenosylmethionine Administration Attenuates Low Brain-Derived Neurotrophic Factor Expression Induced by Chronic Cerebrovascular Hypoperfusion or Beta Amyloid Treatment</atitle><jtitle>Neuroscience bulletin</jtitle><stitle>Neurosci. Bull</stitle><addtitle>Neuroscience Bulletin</addtitle><date>2016-04-01</date><risdate>2016</risdate><volume>32</volume><issue>2</issue><spage>153</spage><epage>161</epage><pages>153-161</pages><issn>1673-7067</issn><eissn>1995-8218</eissn><abstract>Chronic cerebrovascular hypoperfusion is a high-risk factor for Alzheimer＇s disease（AD） as it is conducive to beta amyloid（Ab） over-production. Brainderived 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 50 noncoding exons to produce a heterogeneous population of BDNF m RNAs. 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 Ab intrahippocampal injection rat model were used to explore the expression profiles of all BDNF transcripts in the hippocampus with chronic cerebrovascular hypoperfusion or Ab injection as well as with SAM treatment. We found that the BDNF m RNAs and protein were down-regulated in the hippocampus undergoing chronic cerebrovascular hypoperfusion as well as Ab 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.</abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>26983613</pmid><doi>10.1007/s12264-016-0023-z</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Neuroscience bulletin, 2016-04, Vol.32 (2), p.153-161 |
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| source | MEDLINE; SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Advertising executives Alzheimer's disease Amyloid beta-Peptides - toxicity Analysis of Variance Anatomy Anesthesiology Animals BDNF基因 Biomedical and Life Sciences Biomedicine Brain Brain-Derived Neurotrophic Factor - genetics Brain-Derived Neurotrophic Factor - metabolism Carotid Stenosis - drug therapy Carotid Stenosis - metabolism Carotid Stenosis - pathology Disease Models, Animal Exons - drug effects Exons - physiology Gene Expression Regulation - drug effects Hippocampus - drug effects Hippocampus - metabolism Human Physiology Male Neurology Neuroprotective Agents - therapeutic use Neurosciences Original Original Article Pain Medicine Peptide Fragments - toxicity Rats Rats, Sprague-Dawley RNA, Messenger S-adenosylmethionine S-Adenosylmethionine - therapeutic use S-腺苷甲硫氨酸 Target marketing Time Factors β-淀粉样蛋白 大鼠模型 慢性 脑源性神经营养因子 脑缺血 诱导 |
| title | S-adenosylmethionine Administration Attenuates Low Brain-Derived Neurotrophic Factor Expression Induced by Chronic Cerebrovascular Hypoperfusion or Beta Amyloid Treatment |
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