Progressive Increase in Infarct Size, Neuroinflammation, and Cognitive Deficits in the Presence of High Levels of Amyloid
In the elderly, cerebral ischemia (CI) occurs in the presence of high levels of amyloid. Neuroinflammation plays a critical role in the pathophysiology of Alzheimer's disease and CI. This study examined infarct size, neuroinflammation, and cognitive deficits over time in rat models of Alzheimer...
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| Veröffentlicht in: | Stroke (1970) 2007-12, Vol.38 (12), p.3245-3250 |
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| creator | WHITEHEAD, Shawn N GUANLIANG CHENG HACHINSKI, Vladimir C CECHETTO, David F |
| description | In the elderly, cerebral ischemia (CI) occurs in the presence of high levels of amyloid. Neuroinflammation plays a critical role in the pathophysiology of Alzheimer's disease and CI. This study examined infarct size, neuroinflammation, and cognitive deficits over time in rat models of Alzheimer's disease and CI.
beta-amyloid toxicity was modeled using bilateral intracerebroventricular injections of beta-amyloid 25 to 35 peptides. CI was modeled using unilateral injections of the potent vasoconstrictor, endothelin-1, into the striatum.
Infarct volumes were higher in the presence of amyloid and compared with the CI model alone. In the CI model alone, the infarct volume was significantly smaller 28 days after surgery compared with 7 days after surgery. However, when Alzheimer's disease and CI models were combined, the infarct volume was significantly larger 28 days after surgery compared with 7 days after surgery. The neuroinflammation in the region of the infarct was also significantly increased. The Barnes circular platform test showed time-dependent increases in memory and learning deficits in the beta-amyloid-treated rats that were even greater when beta-amyloid treatment was combined with CI.
CI in the presence of high levels of amyloid results in progressive increases in infarct size, neuroinflammation, and cognitive deficits. |
| doi_str_mv | 10.1161/STROKEAHA.107.492660 |
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beta-amyloid toxicity was modeled using bilateral intracerebroventricular injections of beta-amyloid 25 to 35 peptides. CI was modeled using unilateral injections of the potent vasoconstrictor, endothelin-1, into the striatum.
Infarct volumes were higher in the presence of amyloid and compared with the CI model alone. In the CI model alone, the infarct volume was significantly smaller 28 days after surgery compared with 7 days after surgery. However, when Alzheimer's disease and CI models were combined, the infarct volume was significantly larger 28 days after surgery compared with 7 days after surgery. The neuroinflammation in the region of the infarct was also significantly increased. The Barnes circular platform test showed time-dependent increases in memory and learning deficits in the beta-amyloid-treated rats that were even greater when beta-amyloid treatment was combined with CI.
CI in the presence of high levels of amyloid results in progressive increases in infarct size, neuroinflammation, and cognitive deficits.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/STROKEAHA.107.492660</identifier><identifier>PMID: 17962591</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Alzheimer Disease - pathology ; Amyloid - biosynthesis ; Amyloidosis ; Animals ; Associated diseases and complications ; Biological and medical sciences ; Brain - pathology ; Brain Ischemia - pathology ; Cerebral Infarction - pathology ; Cognition Disorders - pathology ; Diabetes. Impaired glucose tolerance ; Disease Models, Animal ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Humans ; Inflammation - pathology ; Medical sciences ; Memory ; Metabolic diseases ; Nervous System Diseases - pathology ; Neurology ; Other metabolic disorders ; Rats ; Rats, Wistar ; Stroke - pathology ; Time Factors ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 2007-12, Vol.38 (12), p.3245-3250</ispartof><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-a3ba6d6b7749068664275a6b8844ce4751b53bcc0cf1bb55a40283268d2431003</citedby><cites>FETCH-LOGICAL-c449t-a3ba6d6b7749068664275a6b8844ce4751b53bcc0cf1bb55a40283268d2431003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3685,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19876234$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17962591$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WHITEHEAD, Shawn N</creatorcontrib><creatorcontrib>GUANLIANG CHENG</creatorcontrib><creatorcontrib>HACHINSKI, Vladimir C</creatorcontrib><creatorcontrib>CECHETTO, David F</creatorcontrib><title>Progressive Increase in Infarct Size, Neuroinflammation, and Cognitive Deficits in the Presence of High Levels of Amyloid</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>In the elderly, cerebral ischemia (CI) occurs in the presence of high levels of amyloid. Neuroinflammation plays a critical role in the pathophysiology of Alzheimer's disease and CI. This study examined infarct size, neuroinflammation, and cognitive deficits over time in rat models of Alzheimer's disease and CI.
beta-amyloid toxicity was modeled using bilateral intracerebroventricular injections of beta-amyloid 25 to 35 peptides. CI was modeled using unilateral injections of the potent vasoconstrictor, endothelin-1, into the striatum.
Infarct volumes were higher in the presence of amyloid and compared with the CI model alone. In the CI model alone, the infarct volume was significantly smaller 28 days after surgery compared with 7 days after surgery. However, when Alzheimer's disease and CI models were combined, the infarct volume was significantly larger 28 days after surgery compared with 7 days after surgery. The neuroinflammation in the region of the infarct was also significantly increased. The Barnes circular platform test showed time-dependent increases in memory and learning deficits in the beta-amyloid-treated rats that were even greater when beta-amyloid treatment was combined with CI.
CI in the presence of high levels of amyloid results in progressive increases in infarct size, neuroinflammation, and cognitive deficits.</description><subject>Alzheimer Disease - pathology</subject><subject>Amyloid - biosynthesis</subject><subject>Amyloidosis</subject><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Brain Ischemia - pathology</subject><subject>Cerebral Infarction - pathology</subject><subject>Cognition Disorders - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Disease Models, Animal</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Humans</subject><subject>Inflammation - pathology</subject><subject>Medical sciences</subject><subject>Memory</subject><subject>Metabolic diseases</subject><subject>Nervous System Diseases - pathology</subject><subject>Neurology</subject><subject>Other metabolic disorders</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Stroke - pathology</subject><subject>Time Factors</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMlOwzAURS0EgjL8AULewKopnuLEy6oMRVSAGNaR47wUo8QGO61Uvp5UrejqDTr3Lg5C55SMKJX0-u399fnxdjwdjyjJRkIxKckeGtCUiURIlu-jASFcJUwodYSOY_wihDCep4foiGZKslTRAVq9BD8PEKNdAn5wJoCOgK3r91oH0-E3-wtD_ASL4K2rG922urPeDbF2FZ74ubPdOnoDtTW2i-to9wn4pe8EZwD7Gk_t_BPPYAlNXJ_jdtV4W52ig1o3Ec628wR93N2-T6bJ7Pn-YTKeJUYI1SWal1pWsswyoYjMpRQsS7Us81wIAyJLaZny0hhialqWaaoFYTlnMq-Y4LQ3cIKuNr3fwf8sIHZFa6OBptEO_CIWjFCuFGU9KDagCT7GAHXxHWyrw6qgpFgrL_6V95-s2CjvYxfb_kXZQrULbR33wOUW0NHopg7aGRt3nMozybjgfwhGih8</recordid><startdate>20071201</startdate><enddate>20071201</enddate><creator>WHITEHEAD, Shawn N</creator><creator>GUANLIANG CHENG</creator><creator>HACHINSKI, Vladimir C</creator><creator>CECHETTO, David F</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</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>7QO</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20071201</creationdate><title>Progressive Increase in Infarct Size, Neuroinflammation, and Cognitive Deficits in the Presence of High Levels of Amyloid</title><author>WHITEHEAD, Shawn N ; GUANLIANG CHENG ; HACHINSKI, Vladimir C ; CECHETTO, David F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-a3ba6d6b7749068664275a6b8844ce4751b53bcc0cf1bb55a40283268d2431003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Alzheimer Disease - pathology</topic><topic>Amyloid - biosynthesis</topic><topic>Amyloidosis</topic><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Brain Ischemia - pathology</topic><topic>Cerebral Infarction - pathology</topic><topic>Cognition Disorders - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Disease Models, Animal</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Humans</topic><topic>Inflammation - pathology</topic><topic>Medical sciences</topic><topic>Memory</topic><topic>Metabolic diseases</topic><topic>Nervous System Diseases - pathology</topic><topic>Neurology</topic><topic>Other metabolic disorders</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Stroke - pathology</topic><topic>Time Factors</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WHITEHEAD, Shawn N</creatorcontrib><creatorcontrib>GUANLIANG CHENG</creatorcontrib><creatorcontrib>HACHINSKI, Vladimir C</creatorcontrib><creatorcontrib>CECHETTO, David F</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WHITEHEAD, Shawn N</au><au>GUANLIANG CHENG</au><au>HACHINSKI, Vladimir C</au><au>CECHETTO, David F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Progressive Increase in Infarct Size, Neuroinflammation, and Cognitive Deficits in the Presence of High Levels of Amyloid</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2007-12-01</date><risdate>2007</risdate><volume>38</volume><issue>12</issue><spage>3245</spage><epage>3250</epage><pages>3245-3250</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>In the elderly, cerebral ischemia (CI) occurs in the presence of high levels of amyloid. Neuroinflammation plays a critical role in the pathophysiology of Alzheimer's disease and CI. This study examined infarct size, neuroinflammation, and cognitive deficits over time in rat models of Alzheimer's disease and CI.
beta-amyloid toxicity was modeled using bilateral intracerebroventricular injections of beta-amyloid 25 to 35 peptides. CI was modeled using unilateral injections of the potent vasoconstrictor, endothelin-1, into the striatum.
Infarct volumes were higher in the presence of amyloid and compared with the CI model alone. In the CI model alone, the infarct volume was significantly smaller 28 days after surgery compared with 7 days after surgery. However, when Alzheimer's disease and CI models were combined, the infarct volume was significantly larger 28 days after surgery compared with 7 days after surgery. The neuroinflammation in the region of the infarct was also significantly increased. The Barnes circular platform test showed time-dependent increases in memory and learning deficits in the beta-amyloid-treated rats that were even greater when beta-amyloid treatment was combined with CI.
CI in the presence of high levels of amyloid results in progressive increases in infarct size, neuroinflammation, and cognitive deficits.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>17962591</pmid><doi>10.1161/STROKEAHA.107.492660</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Alzheimer Disease - pathology Amyloid - biosynthesis Amyloidosis Animals Associated diseases and complications Biological and medical sciences Brain - pathology Brain Ischemia - pathology Cerebral Infarction - pathology Cognition Disorders - pathology Diabetes. Impaired glucose tolerance Disease Models, Animal Endocrine pancreas. Apud cells (diseases) Endocrinopathies Humans Inflammation - pathology Medical sciences Memory Metabolic diseases Nervous System Diseases - pathology Neurology Other metabolic disorders Rats Rats, Wistar Stroke - pathology Time Factors Vascular diseases and vascular malformations of the nervous system |
| title | Progressive Increase in Infarct Size, Neuroinflammation, and Cognitive Deficits in the Presence of High Levels of Amyloid |
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