Damage to dopamine systems differs between parkinson's disease and alzheimer's disease with parkinsonism
Identifieur interne : 002340 ( Main/Exploration ); précédent : 002339; suivant : 002341Damage to dopamine systems differs between parkinson's disease and alzheimer's disease with parkinsonism
Auteurs : Angela M. Murray [États-Unis] ; Fredric B. Weihmueller [États-Unis] ; John F. Marshall [États-Unis] ; Howard I. Hurtig [États-Unis] ; Gary L. Gottleib [États-Unis] ; Joyce [États-Unis]Source :
- Annals of Neurology [ 0364-5134 ] ; 1995-03.
Abstract
Parkinsonism occurs in approximately 35 to 40% of patients with Alzheimer's disease (AD) even with little or no neuronal degeneration in the substantia nigra, which in idiopathic Parkinson's disease (PD) results in the severe loss of striatal dopamine transporter sites. It is not known if there is a loss of striatal dopamine transporter sites in AD with coexistent parkinsonism (AD/parkinsonism). We quantified the pattern of these sites in the striatum and midbrain of patients with the clinical diagnosis of PD, AD, and AD/parkinsonism in comparison with a group of age‐matched control subjects. We also quantified the number of D2 receptors and the levels of tyrosine hydroxylase in the substantia nigra and ventral tegmental area of same groups. The results showed that in AD the loss of dopamine transporter sites was restricted to the nucleus accumbens. The loss of these sites in the AD/parkinsonism group was more extensive than in the AD group, with the most severe losses in the rostral caudate and putamen and least in the caudal caudate and putamen. While the PD group showed an equally severe reduction in numbers of sites, the caudal to rostral gradient of loss differed from that in the AD/parkinsonism group. The PD group also showed a marked loss of dopamine transporter sites, tyrosine hydroxylase, and D2 autoreceptors (located on dopamine neurons) in the substantia nigra and ventral tegmental area. In contrast, no reductions in dopamine transporter sites, tyrosine hydroxylase, and D2 autoreceptors were observed in the substantia nigra and ventral tegmental area of the AD or AD/parkinsonism groups. Thus, the loss of striatal dopamine transporter sites in AD/parkinsonism may be related to the clinical parkinsonian symptoms. However, the loss is not simply the result of neuronal degeneration in the substantia nigra, but must derive from other processes.
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DOI: 10.1002/ana.410370306
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Gottleib</name></author><author><name sortKey="Joyce" sort="Joyce" uniqKey="Joyce" last="Joyce">Joyce</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0779E99CA796FA022C602D54B22C390B394CDC6A</idno><date when="1995" year="1995">1995</date><idno type="doi">10.1002/ana.410370306</idno><idno type="url">https://api.istex.fr/document/0779E99CA796FA022C602D54B22C390B394CDC6A/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001439</idno><idno type="wicri:Area/Main/Curation">001223</idno><idno type="wicri:Area/Main/Exploration">002340</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Damage to dopamine systems differs between parkinson's disease and alzheimer's disease with parkinsonism</title><author><name sortKey="Murray, Angela M" sort="Murray, Angela M" uniqKey="Murray A" first="Angela M." last="Murray">Angela M. 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Marshall</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Psychobiology, University of California, Irvine</wicri:cityArea></affiliation></author><author><name sortKey="Hurtig, Howard I" sort="Hurtig, Howard I" uniqKey="Hurtig H" first="Howard I." last="Hurtig">Howard I. Hurtig</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Neurology, Graduate Hospital and Hospital of the University of Pennsylvania, Philadelphia</wicri:cityArea></affiliation></author><author><name sortKey="Gottleib, Gary L" sort="Gottleib, Gary L" uniqKey="Gottleib G" first="Gary L." last="Gottleib">Gary L. Gottleib</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Philadelphie</settlement><region type="state">Pennsylvanie</region></placeName><wicri:orgArea>Department of Psychiatry, University of Pennsylvania School of Medicine</wicri:orgArea></affiliation></author><author><name sortKey="Joyce" sort="Joyce" uniqKey="Joyce" last="Joyce">Joyce</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Philadelphie</settlement><region type="state">Pennsylvanie</region></placeName><wicri:orgArea>Department of Psychiatry, University of Pennsylvania School of Medicine</wicri:orgArea></affiliation><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Philadelphie</settlement><region type="state">Pennsylvanie</region></placeName><wicri:orgArea>Department of Pharmacology, University of Pennsylvania School of Medicine</wicri:orgArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-03">1995-03</date><biblScope unit="volume">37</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="300">300</biblScope><biblScope unit="page" to="312">312</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">0779E99CA796FA022C602D54B22C390B394CDC6A</idno><idno type="DOI">10.1002/ana.410370306</idno><idno type="ArticleID">ANA410370306</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinsonism occurs in approximately 35 to 40% of patients with Alzheimer's disease (AD) even with little or no neuronal degeneration in the substantia nigra, which in idiopathic Parkinson's disease (PD) results in the severe loss of striatal dopamine transporter sites. It is not known if there is a loss of striatal dopamine transporter sites in AD with coexistent parkinsonism (AD/parkinsonism). We quantified the pattern of these sites in the striatum and midbrain of patients with the clinical diagnosis of PD, AD, and AD/parkinsonism in comparison with a group of age‐matched control subjects. We also quantified the number of D2 receptors and the levels of tyrosine hydroxylase in the substantia nigra and ventral tegmental area of same groups. The results showed that in AD the loss of dopamine transporter sites was restricted to the nucleus accumbens. The loss of these sites in the AD/parkinsonism group was more extensive than in the AD group, with the most severe losses in the rostral caudate and putamen and least in the caudal caudate and putamen. While the PD group showed an equally severe reduction in numbers of sites, the caudal to rostral gradient of loss differed from that in the AD/parkinsonism group. The PD group also showed a marked loss of dopamine transporter sites, tyrosine hydroxylase, and D2 autoreceptors (located on dopamine neurons) in the substantia nigra and ventral tegmental area. In contrast, no reductions in dopamine transporter sites, tyrosine hydroxylase, and D2 autoreceptors were observed in the substantia nigra and ventral tegmental area of the AD or AD/parkinsonism groups. Thus, the loss of striatal dopamine transporter sites in AD/parkinsonism may be related to the clinical parkinsonian symptoms. However, the loss is not simply the result of neuronal degeneration in the substantia nigra, but must derive from other processes.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li><li>Pennsylvanie</li></region><settlement><li>Philadelphie</li></settlement></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Murray, Angela M" sort="Murray, Angela M" uniqKey="Murray A" first="Angela M." last="Murray">Angela M. Murray</name></region><name sortKey="Gottleib, Gary L" sort="Gottleib, Gary L" uniqKey="Gottleib G" first="Gary L." last="Gottleib">Gary L. Gottleib</name><name sortKey="Hurtig, Howard I" sort="Hurtig, Howard I" uniqKey="Hurtig H" first="Howard I." last="Hurtig">Howard I. Hurtig</name><name sortKey="Joyce" sort="Joyce" uniqKey="Joyce" last="Joyce">Joyce</name><name sortKey="Joyce" sort="Joyce" uniqKey="Joyce" last="Joyce">Joyce</name><name sortKey="Marshall, John F" sort="Marshall, John F" uniqKey="Marshall J" first="John F." last="Marshall">John F. Marshall</name><name sortKey="Weihmueller, Fredric B" sort="Weihmueller, Fredric B" uniqKey="Weihmueller F" first="Fredric B." last="Weihmueller">Fredric B. Weihmueller</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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