Red Blood Cell Abnormalities in Alzheimer Disease
Identifieur interne : 001610 ( Main/Corpus ); précédent : 001609; suivant : 001611Red Blood Cell Abnormalities in Alzheimer Disease
Auteurs : John P. Blass ; Israel Hanin ; Laurie Barclay ; Ursula Kopp ; Michael J. RedingSource :
- Journal of the American Geriatrics Society [ 0002-8614 ] ; 1985-06.
Abstract
In a prospective, double‐blind study of 84 unselected persons in a dementia clinic, the red blood cell/plasma choline ratios were found to be significantly higher in 47 subjects with clinically defined Alzheimer disease (DAT) than in 37 non‐DAT, nondepressed subjects (3.54 ± 0.48 versus 2.04 ± 0.34, p < 0.02). The latter group included intellectually intact subjects as well as patients with other dementias who were comparable to the Alzheimer patients in age, sex, and degree of cognitive impairment. The elevated mean ratio reflected the greater proportion of Alzheimer patients with high red blood cell plasma choline ratios. These elevated ratios appeared to be related to both increases in red cell content and decreases in plasma choline. The authors conclude that the results confirm and extend those previously reported in short series of patients and agree with other evidence that Alzheimer disease has systemic manifestations in nonneural cells, which may be useful in further investigations of the disease's cellular pathophysiology.
Url:
DOI: 10.1111/j.1532-5415.1985.tb07150.x
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Blass</name><affiliation><mods:affiliation>Altschul Laboratory for Dementia Research, Burke Rehabilitation Center, White Plains, New York</mods:affiliation></affiliation></author><author><name sortKey="Hanin, Israel" sort="Hanin, Israel" uniqKey="Hanin I" first="Israel" last="Hanin">Israel Hanin</name><affiliation><mods:affiliation>Western Psychiatric Institute and Clinic, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</mods:affiliation></affiliation></author><author><name sortKey="Barclay, Laurie" sort="Barclay, Laurie" uniqKey="Barclay L" first="Laurie" last="Barclay">Laurie Barclay</name><affiliation><mods:affiliation>Altschul Laboratory for Dementia Research, Burke Rehabilitation Center, White Plains, New York</mods:affiliation></affiliation></author><author><name sortKey="Kopp, Ursula" sort="Kopp, Ursula" uniqKey="Kopp U" first="Ursula" last="Kopp">Ursula Kopp</name><affiliation><mods:affiliation>Western Psychiatric Institute and Clinic, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</mods:affiliation></affiliation></author><author><name sortKey="Reding, Michael J" sort="Reding, Michael J" uniqKey="Reding M" first="Michael J." last="Reding">Michael J. 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Blass</name><affiliation><mods:affiliation>Altschul Laboratory for Dementia Research, Burke Rehabilitation Center, White Plains, New York</mods:affiliation></affiliation></author><author><name sortKey="Hanin, Israel" sort="Hanin, Israel" uniqKey="Hanin I" first="Israel" last="Hanin">Israel Hanin</name><affiliation><mods:affiliation>Western Psychiatric Institute and Clinic, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</mods:affiliation></affiliation></author><author><name sortKey="Barclay, Laurie" sort="Barclay, Laurie" uniqKey="Barclay L" first="Laurie" last="Barclay">Laurie Barclay</name><affiliation><mods:affiliation>Altschul Laboratory for Dementia Research, Burke Rehabilitation Center, White Plains, New York</mods:affiliation></affiliation></author><author><name sortKey="Kopp, Ursula" sort="Kopp, Ursula" uniqKey="Kopp U" first="Ursula" last="Kopp">Ursula Kopp</name><affiliation><mods:affiliation>Western Psychiatric Institute and Clinic, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</mods:affiliation></affiliation></author><author><name sortKey="Reding, Michael J" sort="Reding, Michael J" uniqKey="Reding M" first="Michael J." last="Reding">Michael J. Reding</name><affiliation><mods:affiliation>Altschul Laboratory for Dementia Research, Burke Rehabilitation Center, White Plains, New York</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the American Geriatrics Society</title><idno type="ISSN">0002-8614</idno><idno type="eISSN">1532-5415</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1985-06">1985-06</date><biblScope unit="volume">33</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="401">401</biblScope><biblScope unit="page" to="405">405</biblScope></imprint><idno type="ISSN">0002-8614</idno></series><idno type="istex">1A212BACA9990EA192C3CE506D15D24EA56C6C8E</idno><idno type="DOI">10.1111/j.1532-5415.1985.tb07150.x</idno><idno type="ArticleID">JGS7150</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0002-8614</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In a prospective, double‐blind study of 84 unselected persons in a dementia clinic, the red blood cell/plasma choline ratios were found to be significantly higher in 47 subjects with clinically defined Alzheimer disease (DAT) than in 37 non‐DAT, nondepressed subjects (3.54 ± 0.48 versus 2.04 ± 0.34, p < 0.02). The latter group included intellectually intact subjects as well as patients with other dementias who were comparable to the Alzheimer patients in age, sex, and degree of cognitive impairment. The elevated mean ratio reflected the greater proportion of Alzheimer patients with high red blood cell plasma choline ratios. These elevated ratios appeared to be related to both increases in red cell content and decreases in plasma choline. The authors conclude that the results confirm and extend those previously reported in short series of patients and agree with other evidence that Alzheimer disease has systemic manifestations in nonneural cells, which may be useful in further investigations of the disease's cellular pathophysiology.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>John P. 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affiliationRef="#a2"><personName><givenNames>Ursula</givenNames><familyName>Kopp</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Michael J.</givenNames><familyName>Reding</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Altschul Laboratory for Dementia Research, Burke Rehabilitation Center, White Plains, New York</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Western Psychiatric Institute and Clinic, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><p>In a prospective, double‐blind study of 84 unselected persons in a dementia clinic, the red blood cell/plasma choline ratios were found to be significantly higher in 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The latter group included intellectually intact subjects as well as patients with other dementias who were comparable to the Alzheimer patients in age, sex, and degree of cognitive impairment. The elevated mean ratio reflected the greater proportion of Alzheimer patients with high red blood cell plasma choline ratios. These elevated ratios appeared to be related to both increases in red cell content and decreases in plasma choline. 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The latter group included intellectually intact subjects as well as patients with other dementias who were comparable to the Alzheimer patients in age, sex, and degree of cognitive impairment. The elevated mean ratio reflected the greater proportion of Alzheimer patients with high red blood cell plasma choline ratios. These elevated ratios appeared to be related to both increases in red cell content and decreases in plasma choline. The authors conclude that the results confirm and extend those previously reported in short series of patients and agree with other evidence that Alzheimer disease has systemic manifestations in nonneural cells, which may be useful in further investigations of the disease's cellular pathophysiology.</abstract><relatedItem type="host"><titleInfo><title>Journal of the American Geriatrics Society</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0002-8614</identifier><identifier type="eISSN">1532-5415</identifier><identifier type="DOI">10.1111/(ISSN)1532-5415</identifier><identifier type="PublisherID">JGS</identifier><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>401</start><end>405</end><total>5</total></extent></part></relatedItem><identifier type="istex">1A212BACA9990EA192C3CE506D15D24EA56C6C8E</identifier><identifier type="DOI">10.1111/j.1532-5415.1985.tb07150.x</identifier><identifier type="ArticleID">JGS7150</identifier><accessCondition type="use and reproduction" contentType="copyright">1985 The American Geriatrics Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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