Interaction between a rat model of cerebral ischemia and β-amyloid toxicity: Inflammatory responses
Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Inflammatory mechanisms are involved in AD pathology and stroke and may be the mediator between AD and stroke toxicity. AD was modeled by cerebroventricular injections of beta-amyloid (Abeta[25-35]...
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| Veröffentlicht in: | Stroke (1970) 2005, Vol.36 (1), p.107-112 |
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| container_title | Stroke (1970) |
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| creator | WHITEHEAD, Shawn N HACHINSKI, Vladimir C CECHETTO, David F |
| description | Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Inflammatory mechanisms are involved in AD pathology and stroke and may be the mediator between AD and stroke toxicity.
AD was modeled by cerebroventricular injections of beta-amyloid (Abeta[25-35]) and subcortical lacunar infarcts by striatal endothelin injections. Inflammatory mechanisms were examined using immunohistochemical analysis. Memory and motor tasks were assessed using the Montoya staircase test.
Abeta injections elicited increases in pathological and inflammatory correlates of AD in multiple forebrain sites. Increases in astrocytosis and reactive microglia in the hippocampus were enhanced with the combination of endothelin and Abeta(25-35). Abeta(25-35) treatment decreased performance in the Montoya staircase behavioral test.
The enhanced inflammatory response with Abeta toxicity and ischemia may mediate the inability to improve behavioral performance caused by the stroke. Anti-inflammatory treatment may ameliorate the pathological and behavioral deficits associated with the combination of AD and stroke. |
| doi_str_mv | 10.1161/01.STR.0000149627.30763.f9 |
| format | Article |
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AD was modeled by cerebroventricular injections of beta-amyloid (Abeta[25-35]) and subcortical lacunar infarcts by striatal endothelin injections. Inflammatory mechanisms were examined using immunohistochemical analysis. Memory and motor tasks were assessed using the Montoya staircase test.
Abeta injections elicited increases in pathological and inflammatory correlates of AD in multiple forebrain sites. Increases in astrocytosis and reactive microglia in the hippocampus were enhanced with the combination of endothelin and Abeta(25-35). Abeta(25-35) treatment decreased performance in the Montoya staircase behavioral test.
The enhanced inflammatory response with Abeta toxicity and ischemia may mediate the inability to improve behavioral performance caused by the stroke. Anti-inflammatory treatment may ameliorate the pathological and behavioral deficits associated with the combination of AD and stroke.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.0000149627.30763.f9</identifier><identifier>PMID: 15591213</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Alzheimer Disease - chemically induced ; Alzheimer Disease - etiology ; Alzheimer Disease - pathology ; Amyloid beta-Peptides - administration & dosage ; Animals ; Behavior, Animal ; Biological and medical sciences ; Brain - pathology ; Brain Chemistry ; Brain Ischemia - chemically induced ; Brain Ischemia - complications ; Coloring Agents ; Congo Red ; Disease Models, Animal ; Encephalitis - chemically induced ; Encephalitis - complications ; Endothelins - administration & dosage ; Gliosis - chemically induced ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Immunohistochemistry ; Injections ; Learning ; Male ; Medical sciences ; Motor Skills ; Nervous system (semeiology, syndromes) ; Neurology ; Neuropharmacology ; Neuroprotective agent ; Peptide Fragments - administration & dosage ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 2005, Vol.36 (1), p.107-112</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c321t-6bbb5501ab39fd1bb692842430cd17dc0080be9167dc90156f5456cb886b00cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16392326$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15591213$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WHITEHEAD, Shawn N</creatorcontrib><creatorcontrib>HACHINSKI, Vladimir C</creatorcontrib><creatorcontrib>CECHETTO, David F</creatorcontrib><title>Interaction between a rat model of cerebral ischemia and β-amyloid toxicity: Inflammatory responses</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Inflammatory mechanisms are involved in AD pathology and stroke and may be the mediator between AD and stroke toxicity.
AD was modeled by cerebroventricular injections of beta-amyloid (Abeta[25-35]) and subcortical lacunar infarcts by striatal endothelin injections. Inflammatory mechanisms were examined using immunohistochemical analysis. Memory and motor tasks were assessed using the Montoya staircase test.
Abeta injections elicited increases in pathological and inflammatory correlates of AD in multiple forebrain sites. Increases in astrocytosis and reactive microglia in the hippocampus were enhanced with the combination of endothelin and Abeta(25-35). Abeta(25-35) treatment decreased performance in the Montoya staircase behavioral test.
The enhanced inflammatory response with Abeta toxicity and ischemia may mediate the inability to improve behavioral performance caused by the stroke. Anti-inflammatory treatment may ameliorate the pathological and behavioral deficits associated with the combination of AD and stroke.</description><subject>Alzheimer Disease - chemically induced</subject><subject>Alzheimer Disease - etiology</subject><subject>Alzheimer Disease - pathology</subject><subject>Amyloid beta-Peptides - administration & dosage</subject><subject>Animals</subject><subject>Behavior, Animal</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Brain Chemistry</subject><subject>Brain Ischemia - chemically induced</subject><subject>Brain Ischemia - complications</subject><subject>Coloring Agents</subject><subject>Congo Red</subject><subject>Disease Models, Animal</subject><subject>Encephalitis - chemically induced</subject><subject>Encephalitis - complications</subject><subject>Endothelins - administration & dosage</subject><subject>Gliosis - chemically induced</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Immunohistochemistry</subject><subject>Injections</subject><subject>Learning</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Motor Skills</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Peptide Fragments - administration & dosage</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</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>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMFq3DAQhkVJ6G7SvkIRhfRmRyNZWiu3Epp0IVBI0rOQ5BF1sK2NpKXZ18qD5JnqdBd2LjOH758ZPkK-AqsBFFwyqB8e72s2FzRa8VUt2EqJOugPZAmSN1WjeHtClowJXfFG6wU5y_lp5rlo5UeyACk1cBBL0q2ngsn60seJOix_ESdqabKFjrHDgcZAPSZ0yQ60z_4Pjr2lduro22tlx90Q-46W-NL7vuyu6HoKgx1HW2La0YR5E6eM-RM5DXbI-PnQz8nvmx-P1z-ru1-36-vvd5UXHEqlnHNSMrBO6NCBc0rztuGNYL6DVecZa5lDDWqeNQOpgmyk8q5tlWPMB3FOvu33blJ83mIuZpxfxmGwE8ZtNrASoKXiM3i1B32KOScMZpP60aadAWbeHRsGZnZsjo7Nf8cm6Dn85XBl60bsjtGD1Bm4OAA2ezuEZCff5yOnhOaCK_EPYkmHFA</recordid><startdate>2005</startdate><enddate>2005</enddate><creator>WHITEHEAD, Shawn N</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>7TK</scope></search><sort><creationdate>2005</creationdate><title>Interaction between a rat model of cerebral ischemia and β-amyloid toxicity: Inflammatory responses</title><author>WHITEHEAD, Shawn N ; HACHINSKI, Vladimir C ; CECHETTO, David F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c321t-6bbb5501ab39fd1bb692842430cd17dc0080be9167dc90156f5456cb886b00cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Alzheimer Disease - chemically induced</topic><topic>Alzheimer Disease - etiology</topic><topic>Alzheimer Disease - pathology</topic><topic>Amyloid beta-Peptides - administration & dosage</topic><topic>Animals</topic><topic>Behavior, Animal</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Brain Chemistry</topic><topic>Brain Ischemia - chemically induced</topic><topic>Brain Ischemia - complications</topic><topic>Coloring Agents</topic><topic>Congo Red</topic><topic>Disease Models, Animal</topic><topic>Encephalitis - chemically induced</topic><topic>Encephalitis - complications</topic><topic>Endothelins - administration & dosage</topic><topic>Gliosis - chemically induced</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Immunohistochemistry</topic><topic>Injections</topic><topic>Learning</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Motor Skills</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Neuropharmacology</topic><topic>Neuroprotective agent</topic><topic>Peptide Fragments - administration & dosage</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</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>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>Neurosciences Abstracts</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WHITEHEAD, Shawn N</au><au>HACHINSKI, Vladimir C</au><au>CECHETTO, David F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interaction between a rat model of cerebral ischemia and β-amyloid toxicity: Inflammatory responses</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2005</date><risdate>2005</risdate><volume>36</volume><issue>1</issue><spage>107</spage><epage>112</epage><pages>107-112</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Inflammatory mechanisms are involved in AD pathology and stroke and may be the mediator between AD and stroke toxicity.
AD was modeled by cerebroventricular injections of beta-amyloid (Abeta[25-35]) and subcortical lacunar infarcts by striatal endothelin injections. Inflammatory mechanisms were examined using immunohistochemical analysis. Memory and motor tasks were assessed using the Montoya staircase test.
Abeta injections elicited increases in pathological and inflammatory correlates of AD in multiple forebrain sites. Increases in astrocytosis and reactive microglia in the hippocampus were enhanced with the combination of endothelin and Abeta(25-35). Abeta(25-35) treatment decreased performance in the Montoya staircase behavioral test.
The enhanced inflammatory response with Abeta toxicity and ischemia may mediate the inability to improve behavioral performance caused by the stroke. Anti-inflammatory treatment may ameliorate the pathological and behavioral deficits associated with the combination of AD and stroke.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>15591213</pmid><doi>10.1161/01.STR.0000149627.30763.f9</doi><tpages>6</tpages></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 - chemically induced Alzheimer Disease - etiology Alzheimer Disease - pathology Amyloid beta-Peptides - administration & dosage Animals Behavior, Animal Biological and medical sciences Brain - pathology Brain Chemistry Brain Ischemia - chemically induced Brain Ischemia - complications Coloring Agents Congo Red Disease Models, Animal Encephalitis - chemically induced Encephalitis - complications Endothelins - administration & dosage Gliosis - chemically induced Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Immunohistochemistry Injections Learning Male Medical sciences Motor Skills Nervous system (semeiology, syndromes) Neurology Neuropharmacology Neuroprotective agent Peptide Fragments - administration & dosage Pharmacology. Drug treatments Rats Rats, Wistar Vascular diseases and vascular malformations of the nervous system |
| title | Interaction between a rat model of cerebral ischemia and β-amyloid toxicity: Inflammatory responses |
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