Genetic vulnerability following traumatic brain injury: the role of apolipoprotein E

Apolipoprotein E (APOE) is thought to be responsible for the transportation of lipids within the brain, maintaining structural integrity of the microtubule within the neurone, and assisting with neural transmission. Possession of the APOE ε4 allele has also been shown to influence neuropathological...

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Veröffentlicht in:	Molecular pathology 2003-06, Vol.56 (3), p.132-136
Hauptverfasser:	Nathoo, N, Chetty, R, van Dellen, J R, Barnett, G H
Format:	Artikel
Sprache:	eng
Schlagworte:	Alleles amyloid precursor protein APOE apolipoprotein E Apolipoproteins Apolipoproteins E - genetics Apolipoproteins E - physiology APP Biological and medical sciences Brain Brain Injuries - genetics Genetic aspects Genetic Predisposition to Disease genetic vulnerability Health aspects Humans Injuries Injuries of the nervous system and the skull. Diseases due to physical agents LDL low density lipoprotein Medical sciences outcome Physiological aspects Polymorphism, Genetic Prognosis Reviews Traumas. Diseases due to physical agents traumatic brain injury
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container_title	Molecular pathology
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creator	Nathoo, N Chetty, R van Dellen, J R Barnett, G H
description	Apolipoprotein E (APOE) is thought to be responsible for the transportation of lipids within the brain, maintaining structural integrity of the microtubule within the neurone, and assisting with neural transmission. Possession of the APOE ε4 allele has also been shown to influence neuropathological findings in patients who die from traumatic brain injury, including the accumulation of amyloid β protein. Previous clinical studies reporting varying outcome severities of traumatic brain injury, including cognitive and functional recovery, all support the notion that APOE ε4 allele possession is associated with an unfavourable outcome. Evidence from experimental and clinical brain injury studies confirms that APOE plays an important role in the response of the brain to injury.
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Possession of the APOE ε4 allele has also been shown to influence neuropathological findings in patients who die from traumatic brain injury, including the accumulation of amyloid β protein. Previous clinical studies reporting varying outcome severities of traumatic brain injury, including cognitive and functional recovery, all support the notion that APOE ε4 allele possession is associated with an unfavourable outcome. Evidence from experimental and clinical brain injury studies confirms that APOE plays an important role in the response of the brain to injury.</description><identifier>ISSN: 1366-8714</identifier><identifier>EISSN: 1472-4154</identifier><identifier>DOI: 10.1136/mp.56.3.132</identifier><identifier>PMID: 12782758</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and Association of Clinical Pathologists</publisher><subject>Alleles ; amyloid precursor protein ; APOE ; apolipoprotein E ; Apolipoproteins ; Apolipoproteins E - genetics ; Apolipoproteins E - physiology ; APP ; Biological and medical sciences ; Brain ; Brain Injuries - genetics ; Genetic aspects ; Genetic Predisposition to Disease ; genetic vulnerability ; Health aspects ; Humans ; Injuries ; Injuries of the nervous system and the skull. Diseases due to physical agents ; LDL ; low density lipoprotein ; Medical sciences ; outcome ; Physiological aspects ; Polymorphism, Genetic ; Prognosis ; Reviews ; Traumas. Diseases due to physical agents ; traumatic brain injury</subject><ispartof>Molecular pathology, 2003-06, Vol.56 (3), p.132-136</ispartof><rights>Copyright 2003 Journal of Clinical Pathology</rights><rights>2003 INIST-CNRS</rights><rights>COPYRIGHT 2003 BMJ Publishing Group Ltd.</rights><rights>Copyright © 2003, Journal of Clinical Pathology 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b553t-5de2699d3ef6b5b667e0fe73830e77f1b94c73699898b63fd5e568f94857c1323</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1187307/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1187307/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27915,27916,53782,53784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14852003$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12782758$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nathoo, N</creatorcontrib><creatorcontrib>Chetty, R</creatorcontrib><creatorcontrib>van Dellen, J R</creatorcontrib><creatorcontrib>Barnett, G H</creatorcontrib><title>Genetic vulnerability following traumatic brain injury: the role of apolipoprotein E</title><title>Molecular pathology</title><addtitle>Mol Path</addtitle><description>Apolipoprotein E (APOE) is thought to be responsible for the transportation of lipids within the brain, maintaining structural integrity of the microtubule within the neurone, and assisting with neural transmission. Possession of the APOE ε4 allele has also been shown to influence neuropathological findings in patients who die from traumatic brain injury, including the accumulation of amyloid β protein. Previous clinical studies reporting varying outcome severities of traumatic brain injury, including cognitive and functional recovery, all support the notion that APOE ε4 allele possession is associated with an unfavourable outcome. Evidence from experimental and clinical brain injury studies confirms that APOE plays an important role in the response of the brain to injury.</description><subject>Alleles</subject><subject>amyloid precursor protein</subject><subject>APOE</subject><subject>apolipoprotein E</subject><subject>Apolipoproteins</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E - physiology</subject><subject>APP</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain Injuries - genetics</subject><subject>Genetic aspects</subject><subject>Genetic Predisposition to Disease</subject><subject>genetic vulnerability</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Injuries</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>LDL</subject><subject>low density lipoprotein</subject><subject>Medical sciences</subject><subject>outcome</subject><subject>Physiological aspects</subject><subject>Polymorphism, Genetic</subject><subject>Prognosis</subject><subject>Reviews</subject><subject>Traumas. 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Diseases due to physical agents</topic><topic>LDL</topic><topic>low density lipoprotein</topic><topic>Medical sciences</topic><topic>outcome</topic><topic>Physiological aspects</topic><topic>Polymorphism, Genetic</topic><topic>Prognosis</topic><topic>Reviews</topic><topic>Traumas. Diseases due to physical agents</topic><topic>traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nathoo, N</creatorcontrib><creatorcontrib>Chetty, R</creatorcontrib><creatorcontrib>van Dellen, J R</creatorcontrib><creatorcontrib>Barnett, G H</creatorcontrib><collection>Istex</collection><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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nathoo, N</au><au>Chetty, R</au><au>van Dellen, J R</au><au>Barnett, G H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic vulnerability following traumatic brain injury: the role of apolipoprotein E</atitle><jtitle>Molecular pathology</jtitle><addtitle>Mol Path</addtitle><date>2003-06-01</date><risdate>2003</risdate><volume>56</volume><issue>3</issue><spage>132</spage><epage>136</epage><pages>132-136</pages><issn>1366-8714</issn><eissn>1472-4154</eissn><abstract>Apolipoprotein E (APOE) is thought to be responsible for the transportation of lipids within the brain, maintaining structural integrity of the microtubule within the neurone, and assisting with neural transmission. Possession of the APOE ε4 allele has also been shown to influence neuropathological findings in patients who die from traumatic brain injury, including the accumulation of amyloid β protein. Previous clinical studies reporting varying outcome severities of traumatic brain injury, including cognitive and functional recovery, all support the notion that APOE ε4 allele possession is associated with an unfavourable outcome. Evidence from experimental and clinical brain injury studies confirms that APOE plays an important role in the response of the brain to injury.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and Association of Clinical Pathologists</pub><pmid>12782758</pmid><doi>10.1136/mp.56.3.132</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects	Alleles amyloid precursor protein APOE apolipoprotein E Apolipoproteins Apolipoproteins E - genetics Apolipoproteins E - physiology APP Biological and medical sciences Brain Brain Injuries - genetics Genetic aspects Genetic Predisposition to Disease genetic vulnerability Health aspects Humans Injuries Injuries of the nervous system and the skull. Diseases due to physical agents LDL low density lipoprotein Medical sciences outcome Physiological aspects Polymorphism, Genetic Prognosis Reviews Traumas. Diseases due to physical agents traumatic brain injury
title	Genetic vulnerability following traumatic brain injury: the role of apolipoprotein E
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