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Neuroinflammation in Alzheimer's disease wanes with age
Inflammation is a prominent feature in Alzheimer's disease (AD). It has been proposed that aging has an effect on the function of inflammation in the brain, thereby contributing to the development of age-related diseases like AD. However, the age-dependent relationship between inflammation and...
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Published in: | Journal of neuroinflammation 2011-12, Vol.8 (1), p.171-171 |
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description | Inflammation is a prominent feature in Alzheimer's disease (AD). It has been proposed that aging has an effect on the function of inflammation in the brain, thereby contributing to the development of age-related diseases like AD. However, the age-dependent relationship between inflammation and clinical phenotype of AD has never been investigated.
In this study we have analysed features of the neuroinflammatory response in clinically and pathologically confirmed AD and control cases in relation to age (range 52-97 years). The mid-temporal cortex of 19 controls and 19 AD cases was assessed for the occurrence of microglia and astrocytes by immunohistochemistry using antibodies directed against CD68 (KP1), HLA class II (CR3/43) and glial fibrillary acidic protein (GFAP).
By measuring the area density of immunoreactivity we found significantly more microglia and astrocytes in AD cases younger than 80 years compared to older AD patients. In addition, the presence of KP1, CR3/43 and GFAP decreases significantly with increasing age in AD.
Our data suggest that the association between neuroinflammation and AD is stronger in relatively young patients than in the oldest patients. This age-dependent relationship between inflammation and clinical phenotype of AD has implications for the interpretation of biomarkers and treatment of the disease. |
doi_str_mv | 10.1186/1742-2094-8-171 |
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In this study we have analysed features of the neuroinflammatory response in clinically and pathologically confirmed AD and control cases in relation to age (range 52-97 years). The mid-temporal cortex of 19 controls and 19 AD cases was assessed for the occurrence of microglia and astrocytes by immunohistochemistry using antibodies directed against CD68 (KP1), HLA class II (CR3/43) and glial fibrillary acidic protein (GFAP).
By measuring the area density of immunoreactivity we found significantly more microglia and astrocytes in AD cases younger than 80 years compared to older AD patients. In addition, the presence of KP1, CR3/43 and GFAP decreases significantly with increasing age in AD.
Our data suggest that the association between neuroinflammation and AD is stronger in relatively young patients than in the oldest patients. This age-dependent relationship between inflammation and clinical phenotype of AD has implications for the interpretation of biomarkers and treatment of the disease.</description><identifier>ISSN: 1742-2094</identifier><identifier>EISSN: 1742-2094</identifier><identifier>DOI: 10.1186/1742-2094-8-171</identifier><identifier>PMID: 22152162</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Aged ; Aged, 80 and over ; Aging ; Aging - immunology ; Aging - pathology ; Alzheimer Disease - immunology ; Alzheimer Disease - pathology ; Alzheimer's disease ; Animals ; astrocyte ; Biomarkers ; Biomarkers - metabolism ; Development and progression ; Encephalitis - immunology ; Encephalitis - pathology ; Female ; Frequency distribution ; Genotype & phenotype ; Humans ; Male ; microglia ; Middle Aged ; Pathology ; Risk factors ; Studies</subject><ispartof>Journal of neuroinflammation, 2011-12, Vol.8 (1), p.171-171</ispartof><rights>2011 Hoozemans et al; licensee BioMed Central Ltd.</rights><rights>COPYRIGHT 2011 BioMed Central Ltd.</rights><rights>2011 Hoozemans et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright ©2011 Hoozemans et al; licensee BioMed Central Ltd. 2011 Hoozemans et al; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b611t-f966ce2bcae543ba41c71bc4202ddcc242609e8298a874ab0ec607b1bf7bec0f3</citedby><cites>FETCH-LOGICAL-b611t-f966ce2bcae543ba41c71bc4202ddcc242609e8298a874ab0ec607b1bf7bec0f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248382/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/912937364?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22152162$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hoozemans, Jeroen J M</creatorcontrib><creatorcontrib>Rozemuller, Annemieke J M</creatorcontrib><creatorcontrib>van Haastert, Elise S</creatorcontrib><creatorcontrib>Eikelenboom, Piet</creatorcontrib><creatorcontrib>van Gool, Willem A</creatorcontrib><title>Neuroinflammation in Alzheimer's disease wanes with age</title><title>Journal of neuroinflammation</title><addtitle>J Neuroinflammation</addtitle><description>Inflammation is a prominent feature in Alzheimer's disease (AD). It has been proposed that aging has an effect on the function of inflammation in the brain, thereby contributing to the development of age-related diseases like AD. However, the age-dependent relationship between inflammation and clinical phenotype of AD has never been investigated.
In this study we have analysed features of the neuroinflammatory response in clinically and pathologically confirmed AD and control cases in relation to age (range 52-97 years). The mid-temporal cortex of 19 controls and 19 AD cases was assessed for the occurrence of microglia and astrocytes by immunohistochemistry using antibodies directed against CD68 (KP1), HLA class II (CR3/43) and glial fibrillary acidic protein (GFAP).
By measuring the area density of immunoreactivity we found significantly more microglia and astrocytes in AD cases younger than 80 years compared to older AD patients. In addition, the presence of KP1, CR3/43 and GFAP decreases significantly with increasing age in AD.
Our data suggest that the association between neuroinflammation and AD is stronger in relatively young patients than in the oldest patients. This age-dependent relationship between inflammation and clinical phenotype of AD has implications for the interpretation of biomarkers and treatment of the disease.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging</subject><subject>Aging - immunology</subject><subject>Aging - pathology</subject><subject>Alzheimer Disease - immunology</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>astrocyte</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Development and progression</subject><subject>Encephalitis - immunology</subject><subject>Encephalitis - pathology</subject><subject>Female</subject><subject>Frequency distribution</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Male</subject><subject>microglia</subject><subject>Middle Aged</subject><subject>Pathology</subject><subject>Risk factors</subject><subject>Studies</subject><issn>1742-2094</issn><issn>1742-2094</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp1kk1v1DAQhiMEoqVw5oYiOPSU1h47tnNBWio-KlVwgbNlO5Ndr5K42AkV_fX1krLqoiIfPJp557HnoyheU3JGqRLnVHKogDS8UhWV9ElxvPc8fWAfFS9S2hLCoBbwvDgCoDVQAceF_IpzDH7sejMMZvJhLP1YrvrbDfoB42kqW5_QJCxvzIipvPHTpjRrfFk860yf8NX9fVL8-PTx-8WX6urb58uL1VVlBaVT1TVCOATrDNacWcOpk9Q6DgTa1jngIEiDChpllOTGEnSCSEttJy060rGT4nLhtsFs9XX0g4m_dTBe_3GEuNYmTt71qBlK45hinTOGM9oq2gnWWnDILKkblVnvF9b1bAdsHY5TNP0B9DAy-o1eh1-aAVdMQQZ8WADWh_8ADiMuDHo3BL0bglbZphlyev-LGH7OmCY9-OSw73N_w5x0QxlnSiiRlW__UW7DHMfc7iyChkkmeBa9W0Rrk3uQBxnyy26H1CuQdcMUBZZVZ4-o8mlx8C6M2PnsP0g4XxJcDClF7PZVUqJ3q_dIXW8ednev_7tr7A7RxNMC</recordid><startdate>20111207</startdate><enddate>20111207</enddate><creator>Hoozemans, Jeroen J M</creator><creator>Rozemuller, Annemieke J M</creator><creator>van Haastert, Elise S</creator><creator>Eikelenboom, Piet</creator><creator>van Gool, Willem A</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><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>3V.</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20111207</creationdate><title>Neuroinflammation in Alzheimer's disease wanes with age</title><author>Hoozemans, Jeroen J M ; Rozemuller, Annemieke J M ; van Haastert, Elise S ; Eikelenboom, Piet ; van Gool, Willem A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b611t-f966ce2bcae543ba41c71bc4202ddcc242609e8298a874ab0ec607b1bf7bec0f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging</topic><topic>Aging - immunology</topic><topic>Aging - pathology</topic><topic>Alzheimer Disease - immunology</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>astrocyte</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Development and progression</topic><topic>Encephalitis - immunology</topic><topic>Encephalitis - pathology</topic><topic>Female</topic><topic>Frequency distribution</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Male</topic><topic>microglia</topic><topic>Middle Aged</topic><topic>Pathology</topic><topic>Risk factors</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hoozemans, Jeroen J M</creatorcontrib><creatorcontrib>Rozemuller, Annemieke J M</creatorcontrib><creatorcontrib>van Haastert, Elise S</creatorcontrib><creatorcontrib>Eikelenboom, Piet</creatorcontrib><creatorcontrib>van Gool, Willem A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Publicly Available Content 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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal of neuroinflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hoozemans, Jeroen J M</au><au>Rozemuller, Annemieke J M</au><au>van Haastert, Elise S</au><au>Eikelenboom, Piet</au><au>van Gool, Willem A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroinflammation in Alzheimer's disease wanes with age</atitle><jtitle>Journal of neuroinflammation</jtitle><addtitle>J Neuroinflammation</addtitle><date>2011-12-07</date><risdate>2011</risdate><volume>8</volume><issue>1</issue><spage>171</spage><epage>171</epage><pages>171-171</pages><issn>1742-2094</issn><eissn>1742-2094</eissn><abstract>Inflammation is a prominent feature in Alzheimer's disease (AD). It has been proposed that aging has an effect on the function of inflammation in the brain, thereby contributing to the development of age-related diseases like AD. However, the age-dependent relationship between inflammation and clinical phenotype of AD has never been investigated.
In this study we have analysed features of the neuroinflammatory response in clinically and pathologically confirmed AD and control cases in relation to age (range 52-97 years). The mid-temporal cortex of 19 controls and 19 AD cases was assessed for the occurrence of microglia and astrocytes by immunohistochemistry using antibodies directed against CD68 (KP1), HLA class II (CR3/43) and glial fibrillary acidic protein (GFAP).
By measuring the area density of immunoreactivity we found significantly more microglia and astrocytes in AD cases younger than 80 years compared to older AD patients. In addition, the presence of KP1, CR3/43 and GFAP decreases significantly with increasing age in AD.
Our data suggest that the association between neuroinflammation and AD is stronger in relatively young patients than in the oldest patients. This age-dependent relationship between inflammation and clinical phenotype of AD has implications for the interpretation of biomarkers and treatment of the disease.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>22152162</pmid><doi>10.1186/1742-2094-8-171</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Aged, 80 and over Aging Aging - immunology Aging - pathology Alzheimer Disease - immunology Alzheimer Disease - pathology Alzheimer's disease Animals astrocyte Biomarkers Biomarkers - metabolism Development and progression Encephalitis - immunology Encephalitis - pathology Female Frequency distribution Genotype & phenotype Humans Male microglia Middle Aged Pathology Risk factors Studies |
title | Neuroinflammation in Alzheimer's disease wanes with age |
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