Retinal ganglion cells in Alzheimer's disease and aging
Optic nerve and retinal gangliion cell (GC) degeneration are possible explanations for the poor visul function reported in patients with Alzheimer's disease (AD). We investigated whether GC loss could be attributed to AD compared with control subjects by measuring the spatial density of GC(vell...
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| Veröffentlicht in: | Annals of neurology 1993-03, Vol.33 (3), p.248-257 |
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| container_title | Annals of neurology |
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| creator | Curcio, Christine A. Drucker, David N. |
| description | Optic nerve and retinal gangliion cell (GC) degeneration are possible explanations for the poor visul function reported in patients with Alzheimer's disease (AD). We investigated whether GC loss could be attributed to AD compared with control subjects by measuring the spatial density of GC(vells/mm2) with methods previously used to analyze the GC distribution of young normal retinas. Retinas from 4 autopsy‐confirmed, severely demented partients with AD and 4 age and sex‐matched control subjects (ages, 66‐86 yr for both groups) withould history of dementing or ocular disease were prepared as unstained whold mounts. Therer was no evidence for loss of GC within the central 43 degrees of vision in patients with AD. The densityof GC subserving the central 11 degrees of vision was reduced by one‐fourth in both AD and control eyes compared with retinas from young adults, as was GC density in a wedge of nasal retina. This loss may contribute to deficits in visual function found in aged individuals, whether or not they have dementia. |
| doi_str_mv | 10.1002/ana.410330305 |
| format | Article |
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We investigated whether GC loss could be attributed to AD compared with control subjects by measuring the spatial density of GC(vells/mm2) with methods previously used to analyze the GC distribution of young normal retinas. Retinas from 4 autopsy‐confirmed, severely demented partients with AD and 4 age and sex‐matched control subjects (ages, 66‐86 yr for both groups) withould history of dementing or ocular disease were prepared as unstained whold mounts. Therer was no evidence for loss of GC within the central 43 degrees of vision in patients with AD. The densityof GC subserving the central 11 degrees of vision was reduced by one‐fourth in both AD and control eyes compared with retinas from young adults, as was GC density in a wedge of nasal retina. This loss may contribute to deficits in visual function found in aged individuals, whether or not they have dementia.</description><identifier>ISSN: 0364-5134</identifier><identifier>EISSN: 1531-8249</identifier><identifier>DOI: 10.1002/ana.410330305</identifier><identifier>PMID: 8498808</identifier><identifier>CODEN: ANNED3</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Aged ; Aging - pathology ; Alzheimer Disease - pathology ; Biological and medical sciences ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. 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We investigated whether GC loss could be attributed to AD compared with control subjects by measuring the spatial density of GC(vells/mm2) with methods previously used to analyze the GC distribution of young normal retinas. Retinas from 4 autopsy‐confirmed, severely demented partients with AD and 4 age and sex‐matched control subjects (ages, 66‐86 yr for both groups) withould history of dementing or ocular disease were prepared as unstained whold mounts. Therer was no evidence for loss of GC within the central 43 degrees of vision in patients with AD. The densityof GC subserving the central 11 degrees of vision was reduced by one‐fourth in both AD and control eyes compared with retinas from young adults, as was GC density in a wedge of nasal retina. This loss may contribute to deficits in visual function found in aged individuals, whether or not they have dementia.</description><subject>Adult</subject><subject>Aged</subject><subject>Aging - pathology</subject><subject>Alzheimer Disease - pathology</subject><subject>Biological and medical sciences</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Retinal Ganglion Cells - pathology</subject><issn>0364-5134</issn><issn>1531-8249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1P20AQxVeoiAbKkWMlHyo4GWa938cIUdoqSiXUConLauwdh22dDXgTtfDX11GsiFMvM4f3mzdPj7EzDpccoLrChJeSgxAgQB2wCVeCl7aS7h2bgNCyVFzI9-w4518A4DSHI3ZkpbMW7ISZO1rHhF2xwLTo4ioVDXVdLmIqpt3rI8Ul9Re5CDETZiowhQIXMS0-sMMWu0yn4z5hPz_f_Lj-Us6-3369ns7KRmqnSmxtDcEJ0lTVTSvb2oUahhFqXgUbwAjZQsOVrMgGYzVhBUFAxRVacEacsPOd71O_et5QXvtlzNuImGi1yd4oo7jUegDLHdj0q5x7av1TH5fYv3gOfluUH4ry-6IG_uNovKmXFPb02Mygfxp1zA12bY-piXmPSaM1d1sbs8P-xI5e_v_TT-fTtwHGwDGv6e_-EvvfXhthlL-f33o5mz849w38nfgHk9-OQQ</recordid><startdate>199303</startdate><enddate>199303</enddate><creator>Curcio, Christine A.</creator><creator>Drucker, David N.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Willey-Liss</general><scope>BSCLL</scope><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>7X8</scope></search><sort><creationdate>199303</creationdate><title>Retinal ganglion cells in Alzheimer's disease and aging</title><author>Curcio, Christine A. ; Drucker, David N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4695-af8b0d93e6e2bcf4fb9db0b9ddb12d8d0734f0c1542e8d786ea20d30215a80973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aging - pathology</topic><topic>Alzheimer Disease - pathology</topic><topic>Biological and medical sciences</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Retinal Ganglion Cells - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Curcio, Christine A.</creatorcontrib><creatorcontrib>Drucker, David N.</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><jtitle>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Curcio, Christine A.</au><au>Drucker, David N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Retinal ganglion cells in Alzheimer's disease and aging</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>1993-03</date><risdate>1993</risdate><volume>33</volume><issue>3</issue><spage>248</spage><epage>257</epage><pages>248-257</pages><issn>0364-5134</issn><eissn>1531-8249</eissn><coden>ANNED3</coden><abstract>Optic nerve and retinal gangliion cell (GC) degeneration are possible explanations for the poor visul function reported in patients with Alzheimer's disease (AD). We investigated whether GC loss could be attributed to AD compared with control subjects by measuring the spatial density of GC(vells/mm2) with methods previously used to analyze the GC distribution of young normal retinas. Retinas from 4 autopsy‐confirmed, severely demented partients with AD and 4 age and sex‐matched control subjects (ages, 66‐86 yr for both groups) withould history of dementing or ocular disease were prepared as unstained whold mounts. Therer was no evidence for loss of GC within the central 43 degrees of vision in patients with AD. The densityof GC subserving the central 11 degrees of vision was reduced by one‐fourth in both AD and control eyes compared with retinas from young adults, as was GC density in a wedge of nasal retina. This loss may contribute to deficits in visual function found in aged individuals, whether or not they have dementia.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>8498808</pmid><doi>10.1002/ana.410330305</doi><tpages>10</tpages></addata></record> |
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| identifier | ISSN: 0364-5134 |
| ispartof | Annals of neurology, 1993-03, Vol.33 (3), p.248-257 |
| issn | 0364-5134 1531-8249 |
| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Adult Aged Aging - pathology Alzheimer Disease - pathology Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Humans Male Medical sciences Neurology Retinal Ganglion Cells - pathology |
| title | Retinal ganglion cells in Alzheimer's disease and aging |
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