Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases
Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease. In this study, we examined the immunohistochemical localization of AGEs, amyloid β protein (...
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| Veröffentlicht in: | The American journal of pathology 1998-10, Vol.153 (4), p.1149-1155 |
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| creator | Sasaki, Nobuyuki Fukatsu, Ryo Tsuzuki, Kayo Hayashi, Yorihide Yoshida, Taku Fujii, Nobuhiro Koike, Takao Wakayama, Ikuro Yanagihara, Richard Garruto, Ralph Amano, Naoji Makita, Zenji |
| description | Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease. In this study, we examined the immunohistochemical localization of AGEs, amyloid β protein (Aβ), apolipoprotein E (ApoE), and tau protein in senile plaques, neurofibrillary tangles (NFTs), and cerebral amyloid angiopathy (CAA) in Alzheimer's disease and other neurodegenerative diseases (progressive supranuclear palsy, Pick's disease, and Guamanian amyotrophic lateral sclerosis/Parkinsonism-dementia complex). In most senile plaques (including diffuse plaques) and CAA from Alzheimer's brains, AGE and ApoE were observed together. However, approximately 5% of plaques were AGE positive but Aβ negative, and the vessels without CAA often showed AGE immunoreactivity. In Alzheimer's disease, AGEs were mainly present in intracellular NFTs, whereas ApoE was mainly present in extracellular NFTs. Pick's bodies in Pick's disease and granulovacuolar degeneration in various neurodegenerative diseases were also AGE positive. In non-Alzheimer neurodegenerative diseases, senile plaques and NFTs showed similar findings to those in Alzheimer's disease. These results suggest that AGE may contribute to eventual neuronal dysfunction and death as an important factor in the progression of various neurodegenerative diseases, including Alzheimer's disease. |
| doi_str_mv | 10.1016/S0002-9440(10)65659-3 |
| format | Article |
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In this study, we examined the immunohistochemical localization of AGEs, amyloid β protein (Aβ), apolipoprotein E (ApoE), and tau protein in senile plaques, neurofibrillary tangles (NFTs), and cerebral amyloid angiopathy (CAA) in Alzheimer's disease and other neurodegenerative diseases (progressive supranuclear palsy, Pick's disease, and Guamanian amyotrophic lateral sclerosis/Parkinsonism-dementia complex). In most senile plaques (including diffuse plaques) and CAA from Alzheimer's brains, AGE and ApoE were observed together. However, approximately 5% of plaques were AGE positive but Aβ negative, and the vessels without CAA often showed AGE immunoreactivity. In Alzheimer's disease, AGEs were mainly present in intracellular NFTs, whereas ApoE was mainly present in extracellular NFTs. Pick's bodies in Pick's disease and granulovacuolar degeneration in various neurodegenerative diseases were also AGE positive. In non-Alzheimer neurodegenerative diseases, senile plaques and NFTs showed similar findings to those in Alzheimer's disease. These results suggest that AGE may contribute to eventual neuronal dysfunction and death as an important factor in the progression of various neurodegenerative diseases, including Alzheimer's disease.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>DOI: 10.1016/S0002-9440(10)65659-3</identifier><identifier>PMID: 9777946</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>Bethesda, MD: Elsevier Inc</publisher><subject>Adult ; Aged ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Amyloid beta-Peptides - metabolism ; Amyotrophic Lateral Sclerosis - metabolism ; Amyotrophic Lateral Sclerosis - pathology ; Apolipoproteins E - metabolism ; Biological and medical sciences ; Cerebral Amyloid Angiopathy - metabolism ; Cerebral Amyloid Angiopathy - pathology ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Dementia - metabolism ; Dementia - pathology ; Female ; Glycation End Products, Advanced - metabolism ; Hippocampus - metabolism ; Hippocampus - pathology ; Humans ; Immunoenzyme Techniques ; Male ; Medical sciences ; Middle Aged ; Neurodegenerative Diseases - metabolism ; Neurofibrillary Tangles - metabolism ; Neurofibrillary Tangles - pathology ; Neurology ; Parkinson Disease - metabolism ; Parkinson Disease - pathology ; Plaque, Amyloid - metabolism ; Plaque, Amyloid - pathology ; Regular ; Supranuclear Palsy, Progressive - metabolism ; Supranuclear Palsy, Progressive - pathology ; Syndrome ; tau Proteins - metabolism ; Temporal Lobe - blood supply ; Temporal Lobe - metabolism ; Temporal Lobe - pathology</subject><ispartof>The American journal of pathology, 1998-10, Vol.153 (4), p.1149-1155</ispartof><rights>1998 American Society for Investigative Pathology</rights><rights>1998 INIST-CNRS</rights><rights>Copyright American Society for Investigative Pathology Oct 1998</rights><rights>Copyright © 1998, American Society for Investigative Pathology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c668t-d1c2d6c012a7fb99f4392c41b535ae74b95cb036913c26865562e0dbc222a4333</citedby><cites>FETCH-LOGICAL-c668t-d1c2d6c012a7fb99f4392c41b535ae74b95cb036913c26865562e0dbc222a4333</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/PMC1853056/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0002944010656593$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,3537,27901,27902,53766,53768,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2411224$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9777946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sasaki, Nobuyuki</creatorcontrib><creatorcontrib>Fukatsu, Ryo</creatorcontrib><creatorcontrib>Tsuzuki, Kayo</creatorcontrib><creatorcontrib>Hayashi, Yorihide</creatorcontrib><creatorcontrib>Yoshida, Taku</creatorcontrib><creatorcontrib>Fujii, Nobuhiro</creatorcontrib><creatorcontrib>Koike, Takao</creatorcontrib><creatorcontrib>Wakayama, Ikuro</creatorcontrib><creatorcontrib>Yanagihara, Richard</creatorcontrib><creatorcontrib>Garruto, Ralph</creatorcontrib><creatorcontrib>Amano, Naoji</creatorcontrib><creatorcontrib>Makita, Zenji</creatorcontrib><title>Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease. In this study, we examined the immunohistochemical localization of AGEs, amyloid β protein (Aβ), apolipoprotein E (ApoE), and tau protein in senile plaques, neurofibrillary tangles (NFTs), and cerebral amyloid angiopathy (CAA) in Alzheimer's disease and other neurodegenerative diseases (progressive supranuclear palsy, Pick's disease, and Guamanian amyotrophic lateral sclerosis/Parkinsonism-dementia complex). In most senile plaques (including diffuse plaques) and CAA from Alzheimer's brains, AGE and ApoE were observed together. However, approximately 5% of plaques were AGE positive but Aβ negative, and the vessels without CAA often showed AGE immunoreactivity. In Alzheimer's disease, AGEs were mainly present in intracellular NFTs, whereas ApoE was mainly present in extracellular NFTs. Pick's bodies in Pick's disease and granulovacuolar degeneration in various neurodegenerative diseases were also AGE positive. In non-Alzheimer neurodegenerative diseases, senile plaques and NFTs showed similar findings to those in Alzheimer's disease. These results suggest that AGE may contribute to eventual neuronal dysfunction and death as an important factor in the progression of various neurodegenerative diseases, including Alzheimer's disease.</description><subject>Adult</subject><subject>Aged</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Amyotrophic Lateral Sclerosis - pathology</subject><subject>Apolipoproteins E - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cerebral Amyloid Angiopathy - metabolism</subject><subject>Cerebral Amyloid Angiopathy - pathology</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Dementia - metabolism</subject><subject>Dementia - pathology</subject><subject>Female</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurofibrillary Tangles - metabolism</subject><subject>Neurofibrillary Tangles - pathology</subject><subject>Neurology</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson Disease - pathology</subject><subject>Plaque, Amyloid - metabolism</subject><subject>Plaque, Amyloid - pathology</subject><subject>Regular</subject><subject>Supranuclear Palsy, Progressive - metabolism</subject><subject>Supranuclear Palsy, Progressive - pathology</subject><subject>Syndrome</subject><subject>tau Proteins - metabolism</subject><subject>Temporal Lobe - blood supply</subject><subject>Temporal Lobe - metabolism</subject><subject>Temporal Lobe - pathology</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkk1v1DAQhiMEKkvhJ1SKEKJwCHj8lfgCWpVSkCqKBJw4WI4z2XiVj62dbNX-epzusgIunCx7nnk1o8dJcgLkDRCQb78RQmimOCevgLyWQgqVsQfJAgQVGQUFD5PFAXmcPAlhHa-SFeQoOVJ5nisuF8nPZbU1vcUqvWhvrRnd0KfnfZV-9UM12TGkrk-X7V2DrkN_GtIPLqAJmJrIXI0N-vQLTpHFFfboY_8WfzPhafKoNm3AZ_vzOPnx8fz72afs8uri89nyMrNSFmNWgaWVtASoyetSqZozRS2HUjBhMOelErYkTCpglspCCiEpkqq0lFLDGWPHybtd7mYqO6ws9qM3rd541xl_qwfj9N-V3jV6NWw1FIIRIWPAy32AH64nDKPuXLDYtqbHYQpaKpVDwfIIPv8HXA-T7-NymkKhcsIKGiGxg6wfQvBYHyYBomd1-l6dnr3MT_fq9LzGyZ9rHLr2rmL9xb5ugjVt7aM3Fw4Y5QCU8oid7rDGrZob51GHzrRtDAVt1hsQTHMNwFUk3-9IjHK2Dr0O1uH8GWKXHXU1uP-M_AvfuMKV</recordid><startdate>19981001</startdate><enddate>19981001</enddate><creator>Sasaki, Nobuyuki</creator><creator>Fukatsu, Ryo</creator><creator>Tsuzuki, Kayo</creator><creator>Hayashi, Yorihide</creator><creator>Yoshida, Taku</creator><creator>Fujii, Nobuhiro</creator><creator>Koike, Takao</creator><creator>Wakayama, Ikuro</creator><creator>Yanagihara, Richard</creator><creator>Garruto, Ralph</creator><creator>Amano, Naoji</creator><creator>Makita, Zenji</creator><general>Elsevier Inc</general><general>ASIP</general><general>American Society for Investigative Pathology</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19981001</creationdate><title>Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases</title><author>Sasaki, Nobuyuki ; Fukatsu, Ryo ; Tsuzuki, Kayo ; Hayashi, Yorihide ; Yoshida, Taku ; Fujii, Nobuhiro ; Koike, Takao ; Wakayama, Ikuro ; Yanagihara, Richard ; Garruto, Ralph ; Amano, Naoji ; Makita, Zenji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c668t-d1c2d6c012a7fb99f4392c41b535ae74b95cb036913c26865562e0dbc222a4333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Amyotrophic Lateral Sclerosis - metabolism</topic><topic>Amyotrophic Lateral Sclerosis - pathology</topic><topic>Apolipoproteins E - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cerebral Amyloid Angiopathy - metabolism</topic><topic>Cerebral Amyloid Angiopathy - pathology</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. 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metabolism</topic><topic>Temporal Lobe - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sasaki, Nobuyuki</creatorcontrib><creatorcontrib>Fukatsu, Ryo</creatorcontrib><creatorcontrib>Tsuzuki, Kayo</creatorcontrib><creatorcontrib>Hayashi, Yorihide</creatorcontrib><creatorcontrib>Yoshida, Taku</creatorcontrib><creatorcontrib>Fujii, Nobuhiro</creatorcontrib><creatorcontrib>Koike, Takao</creatorcontrib><creatorcontrib>Wakayama, Ikuro</creatorcontrib><creatorcontrib>Yanagihara, Richard</creatorcontrib><creatorcontrib>Garruto, Ralph</creatorcontrib><creatorcontrib>Amano, Naoji</creatorcontrib><creatorcontrib>Makita, Zenji</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The American journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sasaki, Nobuyuki</au><au>Fukatsu, Ryo</au><au>Tsuzuki, Kayo</au><au>Hayashi, Yorihide</au><au>Yoshida, Taku</au><au>Fujii, Nobuhiro</au><au>Koike, Takao</au><au>Wakayama, Ikuro</au><au>Yanagihara, Richard</au><au>Garruto, Ralph</au><au>Amano, Naoji</au><au>Makita, Zenji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases</atitle><jtitle>The American journal of pathology</jtitle><addtitle>Am J Pathol</addtitle><date>1998-10-01</date><risdate>1998</risdate><volume>153</volume><issue>4</issue><spage>1149</spage><epage>1155</epage><pages>1149-1155</pages><issn>0002-9440</issn><eissn>1525-2191</eissn><coden>AJPAA4</coden><abstract>Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease. In this study, we examined the immunohistochemical localization of AGEs, amyloid β protein (Aβ), apolipoprotein E (ApoE), and tau protein in senile plaques, neurofibrillary tangles (NFTs), and cerebral amyloid angiopathy (CAA) in Alzheimer's disease and other neurodegenerative diseases (progressive supranuclear palsy, Pick's disease, and Guamanian amyotrophic lateral sclerosis/Parkinsonism-dementia complex). In most senile plaques (including diffuse plaques) and CAA from Alzheimer's brains, AGE and ApoE were observed together. However, approximately 5% of plaques were AGE positive but Aβ negative, and the vessels without CAA often showed AGE immunoreactivity. In Alzheimer's disease, AGEs were mainly present in intracellular NFTs, whereas ApoE was mainly present in extracellular NFTs. Pick's bodies in Pick's disease and granulovacuolar degeneration in various neurodegenerative diseases were also AGE positive. In non-Alzheimer neurodegenerative diseases, senile plaques and NFTs showed similar findings to those in Alzheimer's disease. These results suggest that AGE may contribute to eventual neuronal dysfunction and death as an important factor in the progression of various neurodegenerative diseases, including Alzheimer's disease.</abstract><cop>Bethesda, MD</cop><pub>Elsevier Inc</pub><pmid>9777946</pmid><doi>10.1016/S0002-9440(10)65659-3</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The American journal of pathology, 1998-10, Vol.153 (4), p.1149-1155 |
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| subjects | Adult Aged Alzheimer Disease - metabolism Alzheimer Disease - pathology Amyloid beta-Peptides - metabolism Amyotrophic Lateral Sclerosis - metabolism Amyotrophic Lateral Sclerosis - pathology Apolipoproteins E - metabolism Biological and medical sciences Cerebral Amyloid Angiopathy - metabolism Cerebral Amyloid Angiopathy - pathology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dementia - metabolism Dementia - pathology Female Glycation End Products, Advanced - metabolism Hippocampus - metabolism Hippocampus - pathology Humans Immunoenzyme Techniques Male Medical sciences Middle Aged Neurodegenerative Diseases - metabolism Neurofibrillary Tangles - metabolism Neurofibrillary Tangles - pathology Neurology Parkinson Disease - metabolism Parkinson Disease - pathology Plaque, Amyloid - metabolism Plaque, Amyloid - pathology Regular Supranuclear Palsy, Progressive - metabolism Supranuclear Palsy, Progressive - pathology Syndrome tau Proteins - metabolism Temporal Lobe - blood supply Temporal Lobe - metabolism Temporal Lobe - pathology |
| title | Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases |
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