Brain amyloid and cognition in Lewy body diseases
Identifieur interne : 000208 ( Pmc/Checkpoint ); précédent : 000207; suivant : 000209Brain amyloid and cognition in Lewy body diseases
Auteurs : S. N. Gomperts ; J. J. Locascio ; M. Marquie ; A. L. Santarlasci ; D. M. Rentz ; J. Maye ; K. A. Johnson ; J. H. GrowdonSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2012.
Abstract
Many patients with Parkinson disease (PD) develop dementia (PDD), a syndrome that overlaps clinically and pathologically with dementia with Lewy bodies (DLB); PDD and DLB differ chiefly in the relative timing of dementia and parkinsonism. Brain amyloid deposition is an early feature of DLB and may account in part for its early dementia. We sought to confirm this hypothesis and also to determine whether amyloid accumulation contributes to cognitive impairment and dementia in the broad range of parkinsonian diseases.
29 cognitively normal PD, 14 PD subjects with mild cognitive impairment (PD-MCI), 18 with DLB, 12 with PDD and 85 healthy control subjects (HCS) underwent standardized neurologic and neuropsychological examinations and PiB imaging with PET. Apolipoprotein (APOE) genotypes were obtained in many patients. PiB retention was expressed as the distribution volume ratio using a cerebellar tissue reference.
PiB retention was significantly higher in DLB than in any of the other diagnostic groups. PiB retention did not differ across PDD, PD-MCI, PD, and HCS. Amyloid burden increased with age and with the presence of the APOEε4 allele in all patient groups. Only in the DLB group was amyloid deposition associated with impaired cognition.
DLB subjects have higher amyloid burden than subjects with PDD, PD-MCI, PD or HCS; amyloid deposits are linked to cognitive impairment only in DLB. Early amyloid deposits in DLB relative to PDD may account for their difference in the timing of dementia and parkinsonism.
Url:
DOI: 10.1002/mds.25048
PubMed: 22693110
PubMed Central: 3725259
Affiliations:
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<author><name sortKey="Gomperts, S N" sort="Gomperts, S N" uniqKey="Gomperts S" first="S. N." last="Gomperts">S. N. Gomperts</name>
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<author><name sortKey="Locascio, J J" sort="Locascio, J J" uniqKey="Locascio J" first="J. J." last="Locascio">J. J. Locascio</name>
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<author><name sortKey="Marquie, M" sort="Marquie, M" uniqKey="Marquie M" first="M." last="Marquie">M. Marquie</name>
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<author><name sortKey="Santarlasci, A L" sort="Santarlasci, A L" uniqKey="Santarlasci A" first="A. L." last="Santarlasci">A. L. Santarlasci</name>
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<author><name sortKey="Johnson, K A" sort="Johnson, K A" uniqKey="Johnson K" first="K. A." last="Johnson">K. A. Johnson</name>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P1">Many patients with Parkinson disease (PD) develop dementia (PDD), a syndrome that overlaps clinically and pathologically with dementia with Lewy bodies (DLB); PDD and DLB differ chiefly in the relative timing of dementia and parkinsonism. Brain amyloid deposition is an early feature of DLB and may account in part for its early dementia. We sought to confirm this hypothesis and also to determine whether amyloid accumulation contributes to cognitive impairment and dementia in the broad range of parkinsonian diseases.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P2">29 cognitively normal PD, 14 PD subjects with mild cognitive impairment (PD-MCI), 18 with DLB, 12 with PDD and 85 healthy control subjects (HCS) underwent standardized neurologic and neuropsychological examinations and PiB imaging with PET. Apolipoprotein (APOE) genotypes were obtained in many patients. PiB retention was expressed as the distribution volume ratio using a cerebellar tissue reference.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">PiB retention was significantly higher in DLB than in any of the other diagnostic groups. PiB retention did not differ across PDD, PD-MCI, PD, and HCS. Amyloid burden increased with age and with the presence of the APOEε4 allele in all patient groups. Only in the DLB group was amyloid deposition associated with impaired cognition.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">DLB subjects have higher amyloid burden than subjects with PDD, PD-MCI, PD or HCS; amyloid deposits are linked to cognitive impairment only in DLB. Early amyloid deposits in DLB relative to PDD may account for their difference in the timing of dementia and parkinsonism.</p>
</sec>
</div>
</front>
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<journal-id journal-id-type="nlm-ta">Mov Disord</journal-id>
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<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title>Brain amyloid and cognition in Lewy body diseases</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Gomperts</surname>
<given-names>S. N.</given-names>
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<contrib contrib-type="author"><name><surname>Locascio</surname>
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<contrib contrib-type="author"><name><surname>Marquie</surname>
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<contrib contrib-type="author"><name><surname>Rentz</surname>
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<xref ref-type="aff" rid="A2">2</xref>
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<contrib contrib-type="author"><name><surname>Maye</surname>
<given-names>J.</given-names>
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<contrib contrib-type="author"><name><surname>Johnson</surname>
<given-names>K. A.</given-names>
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<contrib contrib-type="author"><name><surname>Growdon</surname>
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<aff id="A1"><label>1</label>
Massachusetts General Hospital</aff>
<aff id="A2"><label>2</label>
Brigham and Women’s Hospital</aff>
<aff id="A3"><label>3</label>
Autonomous University of Barcelona - Medicine Doctoral Studies</aff>
<author-notes><corresp id="cor1">Corresponding author: John H. Growdon, Massachusetts General Hospital, 15 Parkman Street, WAC 729G, Boston, MA 02114</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>2</day>
<month>7</month>
<year>2013</year>
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<pub-date pub-type="epub"><day>12</day>
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<pub-date pub-type="pmc-release"><day>28</day>
<month>7</month>
<year>2013</year>
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<volume>27</volume>
<issue>8</issue>
<fpage>965</fpage>
<lpage>973</lpage>
<abstract><sec id="S1"><title>Background</title>
<p id="P1">Many patients with Parkinson disease (PD) develop dementia (PDD), a syndrome that overlaps clinically and pathologically with dementia with Lewy bodies (DLB); PDD and DLB differ chiefly in the relative timing of dementia and parkinsonism. Brain amyloid deposition is an early feature of DLB and may account in part for its early dementia. We sought to confirm this hypothesis and also to determine whether amyloid accumulation contributes to cognitive impairment and dementia in the broad range of parkinsonian diseases.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P2">29 cognitively normal PD, 14 PD subjects with mild cognitive impairment (PD-MCI), 18 with DLB, 12 with PDD and 85 healthy control subjects (HCS) underwent standardized neurologic and neuropsychological examinations and PiB imaging with PET. Apolipoprotein (APOE) genotypes were obtained in many patients. PiB retention was expressed as the distribution volume ratio using a cerebellar tissue reference.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">PiB retention was significantly higher in DLB than in any of the other diagnostic groups. PiB retention did not differ across PDD, PD-MCI, PD, and HCS. Amyloid burden increased with age and with the presence of the APOEε4 allele in all patient groups. Only in the DLB group was amyloid deposition associated with impaired cognition.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">DLB subjects have higher amyloid burden than subjects with PDD, PD-MCI, PD or HCS; amyloid deposits are linked to cognitive impairment only in DLB. Early amyloid deposits in DLB relative to PDD may account for their difference in the timing of dementia and parkinsonism.</p>
</sec>
</abstract>
<kwd-group><kwd>dementia</kwd>
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<kwd>Parkinson</kwd>
<kwd>amyloid</kwd>
<kwd>PiB</kwd>
</kwd-group>
<funding-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source>
<award-id>U01 AG016976 || AG</award-id>
</award-group>
<award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source>
<award-id>P50 AG005134 || AG</award-id>
</award-group>
<award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source>
<award-id>P50 AG005134 || AG</award-id>
</award-group>
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</article-meta>
</front>
</pmc>
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<name sortKey="Growdon, J H" sort="Growdon, J H" uniqKey="Growdon J" first="J. H." last="Growdon">J. H. Growdon</name>
<name sortKey="Johnson, K A" sort="Johnson, K A" uniqKey="Johnson K" first="K. A." last="Johnson">K. A. Johnson</name>
<name sortKey="Locascio, J J" sort="Locascio, J J" uniqKey="Locascio J" first="J. J." last="Locascio">J. J. Locascio</name>
<name sortKey="Marquie, M" sort="Marquie, M" uniqKey="Marquie M" first="M." last="Marquie">M. Marquie</name>
<name sortKey="Maye, J" sort="Maye, J" uniqKey="Maye J" first="J." last="Maye">J. Maye</name>
<name sortKey="Rentz, D M" sort="Rentz, D M" uniqKey="Rentz D" first="D. M." last="Rentz">D. M. Rentz</name>
<name sortKey="Santarlasci, A L" sort="Santarlasci, A L" uniqKey="Santarlasci A" first="A. L." last="Santarlasci">A. L. Santarlasci</name>
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