Marked increase of ?-amyloid(1?42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury
Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated [beta]-amyloid (A[beta]), which are p...
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| Veröffentlicht in: | Journal of neurology 2004-07, Vol.251 (7), p.870 |
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| creator | Olsson, Annika Csajbok, Ludvig st, Martin H glund, Kina Nyl n, Karin Rosengren, Lars Nellg rd, Bengt Blennow, Kaj |
| description | Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated [beta]-amyloid (A[beta]), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of A[beta] (A[beta] |
| doi_str_mv | 10.1007/s00415-004-0451-y |
| format | Article |
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Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated [beta]-amyloid (A[beta]), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of A[beta] (A[beta]<(1-42)<) and two soluble forms of APP ([alpha]-sAPP and ßsAPP) in ventricular cerebrospinal fluid (VCSF) and A[beta]<(1-42)< in plasma from 28 patients in a serial samples 0-11 days after TBI. The levels of [alpha]-sAPP, ß-sAPP and A[beta]<(1-42)< were determined using ELISA assays. After TBI, there was a significant stepwise increase in VCSF-A[beta]<(1-42)< up to 1173 % from day 0-1 to day 5-6 and in VCSF-[beta]-sAPP up to 2033 % increase from day 0-1 to day 7-11. There was also a slight but significant increase of VCSF-[beta]-sAPP from day 0-1 to day 5-6 and day 7-11. By contrast, the plasma- A[beta]<(1-42)< level is unchanged after injury. The marked increase in VCSFA[beta]<( 1-42)< implies that increased A[beta] expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma-A[beta]<(1-42)< in contrast to the marked increase in VCSF-A[beta]<(1-42)< after severe TBI, supports the suggestion that plasma A[beta]<(1-42)< does not reflect A[beta] metabolism in the central nervous system (CNS).]]></description><identifier>ISSN: 0340-5354</identifier><identifier>EISSN: 1432-1459</identifier><identifier>DOI: 10.1007/s00415-004-0451-y</identifier><language>eng</language><publisher>Heidelberg: Springer Nature B.V</publisher><subject>Alzheimer's disease ; Cerebrospinal fluid ; Glasgow Coma Scale ; Head injuries ; Intracranial pressure ; Metabolism ; Nervous system ; Neurology ; Neurosciences ; Patients ; Peptides ; Plasma ; Proteins ; Trauma ; Traumatic brain injury</subject><ispartof>Journal of neurology, 2004-07, Vol.251 (7), p.870</ispartof><rights>Copyright Springer-Verlag 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1172-fcb009091fcc8eee4d8724a9f9b5e72d34fb8baadb12438425b760a4c06aa7e73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids></links><search><creatorcontrib>Olsson, Annika</creatorcontrib><creatorcontrib>Csajbok, Ludvig</creatorcontrib><creatorcontrib>st, Martin</creatorcontrib><creatorcontrib>H glund, Kina</creatorcontrib><creatorcontrib>Nyl n, Karin</creatorcontrib><creatorcontrib>Rosengren, Lars</creatorcontrib><creatorcontrib>Nellg rd, Bengt</creatorcontrib><creatorcontrib>Blennow, Kaj</creatorcontrib><title>Marked increase of ?-amyloid(1?42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury</title><title>Journal of neurology</title><description><![CDATA[Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated [beta]-amyloid (A[beta]), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of A[beta] (A[beta]<(1-42)<) and two soluble forms of APP ([alpha]-sAPP and ßsAPP) in ventricular cerebrospinal fluid (VCSF) and A[beta]<(1-42)< in plasma from 28 patients in a serial samples 0-11 days after TBI. The levels of [alpha]-sAPP, ß-sAPP and A[beta]<(1-42)< were determined using ELISA assays. After TBI, there was a significant stepwise increase in VCSF-A[beta]<(1-42)< up to 1173 % from day 0-1 to day 5-6 and in VCSF-[beta]-sAPP up to 2033 % increase from day 0-1 to day 7-11. There was also a slight but significant increase of VCSF-[beta]-sAPP from day 0-1 to day 5-6 and day 7-11. By contrast, the plasma- A[beta]<(1-42)< level is unchanged after injury. The marked increase in VCSFA[beta]<( 1-42)< implies that increased A[beta] expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma-A[beta]<(1-42)< in contrast to the marked increase in VCSF-A[beta]<(1-42)< after severe TBI, supports the suggestion that plasma A[beta]<(1-42)< does not reflect A[beta] metabolism in the central nervous system (CNS).]]></description><subject>Alzheimer's disease</subject><subject>Cerebrospinal fluid</subject><subject>Glasgow Coma Scale</subject><subject>Head injuries</subject><subject>Intracranial pressure</subject><subject>Metabolism</subject><subject>Nervous system</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Patients</subject><subject>Peptides</subject><subject>Plasma</subject><subject>Proteins</subject><subject>Trauma</subject><subject>Traumatic brain injury</subject><issn>0340-5354</issn><issn>1432-1459</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNotUMtO5EAMbCGQGB4fwK3FCQ69636EJCeEEI-VWHGBc8vpuKUMmWRwJ0j5An6bhuFiW64qq1xCnGn4owHKvwnA6ULlqsAVWi17YqWdNUq7ot4XK7AOVGELdyiOUloDQJWBlfj8j_xGreyGwISJ5BjltcLN0o9de6GvnbmUOLTydyO3TGHmNHKexom6ISvlBw0Td2HukWUgpobHtO0G7GXs5yzCOBHLRB8ZkxPjvMGpC7Jh_NGvZ15OxEHEPtHpbz8Wr_d3L7eP6un54d_tzZMKWpdGxdAA1FDrGEJFRK6tSuOwjnVTUGla62JTNYhto42zlTNFU14BugBXiCWV9lic7-5m--8zpcmvx5mz1eSNrrS1dWkySe9IIT-SmKLfcrdBXrwG_x2338Xtc_XfcfvFfgGH-HWY</recordid><startdate>200407</startdate><enddate>200407</enddate><creator>Olsson, Annika</creator><creator>Csajbok, Ludvig</creator><creator>st, Martin</creator><creator>H glund, Kina</creator><creator>Nyl n, Karin</creator><creator>Rosengren, Lars</creator><creator>Nellg rd, Bengt</creator><creator>Blennow, Kaj</creator><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>200407</creationdate><title>Marked increase of ?-amyloid(1?42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury</title><author>Olsson, Annika ; Csajbok, Ludvig ; st, Martin ; H glund, Kina ; Nyl n, Karin ; Rosengren, Lars ; Nellg rd, Bengt ; Blennow, Kaj</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1172-fcb009091fcc8eee4d8724a9f9b5e72d34fb8baadb12438425b760a4c06aa7e73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Alzheimer's disease</topic><topic>Cerebrospinal fluid</topic><topic>Glasgow Coma Scale</topic><topic>Head injuries</topic><topic>Intracranial pressure</topic><topic>Metabolism</topic><topic>Nervous system</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Patients</topic><topic>Peptides</topic><topic>Plasma</topic><topic>Proteins</topic><topic>Trauma</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Olsson, Annika</creatorcontrib><creatorcontrib>Csajbok, Ludvig</creatorcontrib><creatorcontrib>st, Martin</creatorcontrib><creatorcontrib>H glund, Kina</creatorcontrib><creatorcontrib>Nyl n, Karin</creatorcontrib><creatorcontrib>Rosengren, Lars</creatorcontrib><creatorcontrib>Nellg rd, Bengt</creatorcontrib><creatorcontrib>Blennow, Kaj</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Journal of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Olsson, Annika</au><au>Csajbok, Ludvig</au><au>st, Martin</au><au>H glund, Kina</au><au>Nyl n, Karin</au><au>Rosengren, Lars</au><au>Nellg rd, Bengt</au><au>Blennow, Kaj</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Marked increase of ?-amyloid(1?42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury</atitle><jtitle>Journal of neurology</jtitle><date>2004-07</date><risdate>2004</risdate><volume>251</volume><issue>7</issue><spage>870</spage><pages>870-</pages><issn>0340-5354</issn><eissn>1432-1459</eissn><abstract><![CDATA[Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated [beta]-amyloid (A[beta]), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of A[beta] (A[beta]<(1-42)<) and two soluble forms of APP ([alpha]-sAPP and ßsAPP) in ventricular cerebrospinal fluid (VCSF) and A[beta]<(1-42)< in plasma from 28 patients in a serial samples 0-11 days after TBI. The levels of [alpha]-sAPP, ß-sAPP and A[beta]<(1-42)< were determined using ELISA assays. After TBI, there was a significant stepwise increase in VCSF-A[beta]<(1-42)< up to 1173 % from day 0-1 to day 5-6 and in VCSF-[beta]-sAPP up to 2033 % increase from day 0-1 to day 7-11. There was also a slight but significant increase of VCSF-[beta]-sAPP from day 0-1 to day 5-6 and day 7-11. By contrast, the plasma- A[beta]<(1-42)< level is unchanged after injury. The marked increase in VCSFA[beta]<( 1-42)< implies that increased A[beta] expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma-A[beta]<(1-42)< in contrast to the marked increase in VCSF-A[beta]<(1-42)< after severe TBI, supports the suggestion that plasma A[beta]<(1-42)< does not reflect A[beta] metabolism in the central nervous system (CNS).]]></abstract><cop>Heidelberg</cop><pub>Springer Nature B.V</pub><doi>10.1007/s00415-004-0451-y</doi></addata></record> |
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| subjects | Alzheimer's disease Cerebrospinal fluid Glasgow Coma Scale Head injuries Intracranial pressure Metabolism Nervous system Neurology Neurosciences Patients Peptides Plasma Proteins Trauma Traumatic brain injury |
| title | Marked increase of ?-amyloid(1?42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury |
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