Synaptic proteins, neuropathology and cognitive status in the oldest-old

Abstract An increasing number of individuals in our population are surviving to over 90 years and a subset is at risk for developing dementia. However, senile plaque and neurofibrillary tangle pathology do not consistently differentiate individuals with and without dementia. Synaptic protein loss is...

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Veröffentlicht in:Neurobiology of aging 2009-07, Vol.30 (7), p.1125-1134
Hauptverfasser: Head, Elizabeth, Corrada, Maria M, Kahle-Wrobleski, Kristin, Kim, Ronald C, Sarsoza, Floyd, Goodus, Matthew, Kawas, Claudia H
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container_end_page 1134
container_issue 7
container_start_page 1125
container_title Neurobiology of aging
container_volume 30
creator Head, Elizabeth
Corrada, Maria M
Kahle-Wrobleski, Kristin
Kim, Ronald C
Sarsoza, Floyd
Goodus, Matthew
Kawas, Claudia H
description Abstract An increasing number of individuals in our population are surviving to over 90 years and a subset is at risk for developing dementia. However, senile plaque and neurofibrillary tangle pathology do not consistently differentiate individuals with and without dementia. Synaptic protein loss is a feature of aging and dementia and may dissociate 90+ individuals with and without dementia. Synaptophysin (SYN), postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were studied in the frontal cortex of an autopsy series of 32 prospectively followed individuals (92–105 years) with a range of cognitive function. SYN protein levels were decreased in individuals with dementia and increased in those with clinical signs of cognitive impairment insufficient for a diagnosis of dementia. SYN but neither PSD-95 nor GAP-43 protein levels were significantly correlated with mini-mental status examination (MMSE) scores. Frontal cortex SYN protein levels may protect neuronal function in oldest-old individuals and reflect compensatory responses that may be involved with maintaining cognition.
doi_str_mv 10.1016/j.neurobiolaging.2007.10.001
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However, senile plaque and neurofibrillary tangle pathology do not consistently differentiate individuals with and without dementia. Synaptic protein loss is a feature of aging and dementia and may dissociate 90+ individuals with and without dementia. Synaptophysin (SYN), postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were studied in the frontal cortex of an autopsy series of 32 prospectively followed individuals (92–105 years) with a range of cognitive function. SYN protein levels were decreased in individuals with dementia and increased in those with clinical signs of cognitive impairment insufficient for a diagnosis of dementia. SYN but neither PSD-95 nor GAP-43 protein levels were significantly correlated with mini-mental status examination (MMSE) scores. 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Transplantation</subject><subject>Disease Progression</subject><subject>Disks Large Homolog 4 Protein</subject><subject>Female</subject><subject>Frontal Lobe - metabolism</subject><subject>Frontal Lobe - pathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GAP-43 Protein - analysis</subject><subject>GAP-43 Protein - metabolism</subject><subject>Growth-associated protein-43 (GAP-43)</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Intracellular Signaling Peptides and Proteins - analysis</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Male</subject><subject>Membrane Proteins - analysis</subject><subject>Membrane Proteins - metabolism</subject><subject>MMSE</subject><subject>Neurology</subject><subject>Neuropsychological Tests</subject><subject>Oldest-old</subject><subject>Postsynaptic density (PSD)</subject><subject>Prospective Studies</subject><subject>Synaptic Membranes - metabolism</subject><subject>Synaptophysin (SYN)</subject><subject>Synaptophysin - analysis</subject><subject>Synaptophysin - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk9v1DAQxS0EotvCV0A5AKdmGTt_HEuoEqooRarEob1bjjPJesnawXZW2m-Pw64K5QKnOcxvnp_nDSFvKawp0PrDdm1x9q41blSDscOaAfDUWgPQZ2RFq6rJaSn4c7ICKnheVg2ckfMQtpDAktcvyRltAGoqihW5vT9YNUWjs8m7iMaGy-yX_qTixo1uOGTKdpl2gzXR7DELUcU5ZMZmcYOZGzsMMU_lFXnRqzHg61O9IA83nx-ub_O7b1--Xn-6y3UNIuaMVaiV1rRQHetb2lBet8lWj0WrRNl1AEJBW7eFajUvmrKjSlHs27KkFWuKC3J1lJ3mdoedRhu9GuXkzU75g3TKyKcdazZycHvJmagor5LA-5OAdz_mZF7uTNA4jsqim4OsOVueZf8E09prAY1I4McjqL0LwWP_6IaCXCKTW_k0smWWL90UWRp_8-ePfg-fMkrAuxOgglZj75XVJjxyrBCsrIqFuzlymNa_N-hl0Aatxs541FF2zvyvo6u_hPRorElvf8cDhq2bvU0RSyoDkyDvlzNbrgw4QAmMFT8BuiTUzA</recordid><startdate>20090701</startdate><enddate>20090701</enddate><creator>Head, Elizabeth</creator><creator>Corrada, Maria M</creator><creator>Kahle-Wrobleski, Kristin</creator><creator>Kim, Ronald C</creator><creator>Sarsoza, Floyd</creator><creator>Goodus, Matthew</creator><creator>Kawas, Claudia H</creator><general>Elsevier Inc</general><general>Elsevier</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><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090701</creationdate><title>Synaptic proteins, neuropathology and cognitive status in the oldest-old</title><author>Head, Elizabeth ; Corrada, Maria M ; Kahle-Wrobleski, Kristin ; Kim, Ronald C ; Sarsoza, Floyd ; Goodus, Matthew ; Kawas, Claudia H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c609t-225ecacc13ad2fb18176b074fe3ba94dd009a0b6b3abc7384d1aa1efb4415283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Aged, 80 and over</topic><topic>Aging - metabolism</topic><topic>Aging - pathology</topic><topic>Aging - psychology</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - analysis</topic><topic>Biomarkers - metabolism</topic><topic>Clinico-pathology correlation</topic><topic>Cognition Disorders - metabolism</topic><topic>Cognition Disorders - pathology</topic><topic>Cognition Disorders - psychology</topic><topic>Cognitively impaired not demented</topic><topic>Cohort Studies</topic><topic>Compensatory response</topic><topic>Dementia</topic><topic>Dementia - metabolism</topic><topic>Dementia - pathology</topic><topic>Dementia - psychology</topic><topic>Development. Senescence. Regeneration. Transplantation</topic><topic>Disease Progression</topic><topic>Disks Large Homolog 4 Protein</topic><topic>Female</topic><topic>Frontal Lobe - metabolism</topic><topic>Frontal Lobe - pathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GAP-43 Protein - analysis</topic><topic>GAP-43 Protein - metabolism</topic><topic>Growth-associated protein-43 (GAP-43)</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Intracellular Signaling Peptides and Proteins - analysis</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Male</topic><topic>Membrane Proteins - analysis</topic><topic>Membrane Proteins - metabolism</topic><topic>MMSE</topic><topic>Neurology</topic><topic>Neuropsychological Tests</topic><topic>Oldest-old</topic><topic>Postsynaptic density (PSD)</topic><topic>Prospective Studies</topic><topic>Synaptic Membranes - metabolism</topic><topic>Synaptophysin (SYN)</topic><topic>Synaptophysin - analysis</topic><topic>Synaptophysin - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Head, Elizabeth</creatorcontrib><creatorcontrib>Corrada, Maria M</creatorcontrib><creatorcontrib>Kahle-Wrobleski, Kristin</creatorcontrib><creatorcontrib>Kim, Ronald C</creatorcontrib><creatorcontrib>Sarsoza, Floyd</creatorcontrib><creatorcontrib>Goodus, Matthew</creatorcontrib><creatorcontrib>Kawas, Claudia H</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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Head, Elizabeth</au><au>Corrada, Maria M</au><au>Kahle-Wrobleski, Kristin</au><au>Kim, Ronald C</au><au>Sarsoza, Floyd</au><au>Goodus, Matthew</au><au>Kawas, Claudia H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synaptic proteins, neuropathology and cognitive status in the oldest-old</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2009-07-01</date><risdate>2009</risdate><volume>30</volume><issue>7</issue><spage>1125</spage><epage>1134</epage><pages>1125-1134</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><coden>NEAGDO</coden><abstract>Abstract An increasing number of individuals in our population are surviving to over 90 years and a subset is at risk for developing dementia. However, senile plaque and neurofibrillary tangle pathology do not consistently differentiate individuals with and without dementia. Synaptic protein loss is a feature of aging and dementia and may dissociate 90+ individuals with and without dementia. Synaptophysin (SYN), postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were studied in the frontal cortex of an autopsy series of 32 prospectively followed individuals (92–105 years) with a range of cognitive function. SYN protein levels were decreased in individuals with dementia and increased in those with clinical signs of cognitive impairment insufficient for a diagnosis of dementia. SYN but neither PSD-95 nor GAP-43 protein levels were significantly correlated with mini-mental status examination (MMSE) scores. Frontal cortex SYN protein levels may protect neuronal function in oldest-old individuals and reflect compensatory responses that may be involved with maintaining cognition.</abstract><cop>London</cop><pub>Elsevier Inc</pub><pmid>18006193</pmid><doi>10.1016/j.neurobiolaging.2007.10.001</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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subjects Aged, 80 and over
Aging - metabolism
Aging - pathology
Aging - psychology
Biological and medical sciences
Biomarkers - analysis
Biomarkers - metabolism
Clinico-pathology correlation
Cognition Disorders - metabolism
Cognition Disorders - pathology
Cognition Disorders - psychology
Cognitively impaired not demented
Cohort Studies
Compensatory response
Dementia
Dementia - metabolism
Dementia - pathology
Dementia - psychology
Development. Senescence. Regeneration. Transplantation
Disease Progression
Disks Large Homolog 4 Protein
Female
Frontal Lobe - metabolism
Frontal Lobe - pathology
Fundamental and applied biological sciences. Psychology
GAP-43 Protein - analysis
GAP-43 Protein - metabolism
Growth-associated protein-43 (GAP-43)
Humans
Internal Medicine
Intracellular Signaling Peptides and Proteins - analysis
Intracellular Signaling Peptides and Proteins - metabolism
Male
Membrane Proteins - analysis
Membrane Proteins - metabolism
MMSE
Neurology
Neuropsychological Tests
Oldest-old
Postsynaptic density (PSD)
Prospective Studies
Synaptic Membranes - metabolism
Synaptophysin (SYN)
Synaptophysin - analysis
Synaptophysin - metabolism
Vertebrates: nervous system and sense organs
title Synaptic proteins, neuropathology and cognitive status in the oldest-old
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