Comparative alterations of nicotinic and muscarinic binding sites in Alzheimer's and Parkinson's diseases.
Identifieur interne : 001A82 ( PubMed/Corpus ); précédent : 001A81; suivant : 001A83Comparative alterations of nicotinic and muscarinic binding sites in Alzheimer's and Parkinson's diseases.
Auteurs : I. Aubert ; D M Araujo ; D. Cécyre ; Y. Robitaille ; S. Gauthier ; R. QuirionSource :
- Journal of neurochemistry [ 0022-3042 ] ; 1992.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Choline O-Acetyltransferase, Muscarine, Nicotine.
- enzymology : Brain.
- metabolism : Alzheimer Disease, Brain, Parkinson Disease.
- Aged, Binding Sites, Female, Humans, Male.
Abstract
We have recently reported on the differential alterations of various cholinergic markers in cortical and subcortical regions in Alzheimer's disease (AD). The main purpose of the present study was to determine if cholinergic deficits observed in patients with AD are unique to this disorder or can be generalized to others such as idiopathic Parkinson's disease (PD) and PD with Alzheimer-type dementia (PD/AD). Muscarinic M1, M2, and nicotinic receptor binding parameters (KD and Bmax) were determined in various cortical and subcortical areas using selective radioligands ([3H]pirenzepine, [3H]AF-DX 116, and N[3H]methylcarbamylcholine). Choline acetyltransferase activity was also determined as a marker of the integrity of cholinergic innervation. Alterations of cholinergic markers are comparable in cortical areas in AD, PD, and PD/AD brains. In frontal and temporal cortices, as well as in the hippocampus, choline acetyltransferase activity and binding capacities of M2 and nicotinic binding sites are similarly decreased in these three disorders compared with age-matched control values. M1 receptor binding parameters are not significantly modified in cortical areas in patients with these disorders. In contrast, important differences between AD and PD brain tissues are found in subcortical areas such as the striatum and the thalamus. The density of M1 sites is significantly increased in striatal areas only in patients with AD, whereas densities of nicotinic sites are decreased in thalamus and striatum in PD and PD/AD, but not AD, brain tissues. The binding capacity of M2 sites is apparently unchanged in subcortical areas in all three disorders, although tendencies toward reductions are observed in the striatum of PD and PD/AD patients. Thus, although comparable alterations of various cholinergic markers are observed in cortical areas in the three neurological disorders investigated in the present study, important differences are seen in subcortical areas. This may be relevant to the respective etiological and clinical profiles of AD and PD.
PubMed: 1729398
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Comparative alterations of nicotinic and muscarinic binding sites in Alzheimer's and Parkinson's diseases.</title><author><name sortKey="Aubert, I" sort="Aubert, I" uniqKey="Aubert I" first="I" last="Aubert">I. Aubert</name><affiliation><nlm:affiliation>Department of Neurology, McGill University, Montreal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Araujo, D M" sort="Araujo, D M" uniqKey="Araujo D" first="D M" last="Araujo">D M Araujo</name></author><author><name sortKey="Cecyre, D" sort="Cecyre, D" uniqKey="Cecyre D" first="D" last="Cécyre">D. Cécyre</name></author><author><name sortKey="Robitaille, Y" sort="Robitaille, Y" uniqKey="Robitaille Y" first="Y" last="Robitaille">Y. Robitaille</name></author><author><name sortKey="Gauthier, S" sort="Gauthier, S" uniqKey="Gauthier S" first="S" last="Gauthier">S. Gauthier</name></author><author><name sortKey="Quirion, R" sort="Quirion, R" uniqKey="Quirion R" first="R" last="Quirion">R. Quirion</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1992">1992</date><idno type="RBID">pubmed:1729398</idno><idno type="pmid">1729398</idno><idno type="wicri:Area/PubMed/Corpus">001A82</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001A82</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Comparative alterations of nicotinic and muscarinic binding sites in Alzheimer's and Parkinson's diseases.</title><author><name sortKey="Aubert, I" sort="Aubert, I" uniqKey="Aubert I" first="I" last="Aubert">I. Aubert</name><affiliation><nlm:affiliation>Department of Neurology, McGill University, Montreal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Araujo, D M" sort="Araujo, D M" uniqKey="Araujo D" first="D M" last="Araujo">D M Araujo</name></author><author><name sortKey="Cecyre, D" sort="Cecyre, D" uniqKey="Cecyre D" first="D" last="Cécyre">D. Cécyre</name></author><author><name sortKey="Robitaille, Y" sort="Robitaille, Y" uniqKey="Robitaille Y" first="Y" last="Robitaille">Y. Robitaille</name></author><author><name sortKey="Gauthier, S" sort="Gauthier, S" uniqKey="Gauthier S" first="S" last="Gauthier">S. Gauthier</name></author><author><name sortKey="Quirion, R" sort="Quirion, R" uniqKey="Quirion R" first="R" last="Quirion">R. Quirion</name></author></analytic><series><title level="j">Journal of neurochemistry</title><idno type="ISSN">0022-3042</idno><imprint><date when="1992" type="published">1992</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Alzheimer Disease (metabolism)</term><term>Binding Sites</term><term>Brain (enzymology)</term><term>Brain (metabolism)</term><term>Choline O-Acetyltransferase (metabolism)</term><term>Female</term><term>Humans</term><term>Male</term><term>Muscarine (metabolism)</term><term>Nicotine (metabolism)</term><term>Parkinson Disease (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Choline O-Acetyltransferase</term><term>Muscarine</term><term>Nicotine</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Binding Sites</term><term>Female</term><term>Humans</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We have recently reported on the differential alterations of various cholinergic markers in cortical and subcortical regions in Alzheimer's disease (AD). The main purpose of the present study was to determine if cholinergic deficits observed in patients with AD are unique to this disorder or can be generalized to others such as idiopathic Parkinson's disease (PD) and PD with Alzheimer-type dementia (PD/AD). Muscarinic M1, M2, and nicotinic receptor binding parameters (KD and Bmax) were determined in various cortical and subcortical areas using selective radioligands ([3H]pirenzepine, [3H]AF-DX 116, and N[3H]methylcarbamylcholine). Choline acetyltransferase activity was also determined as a marker of the integrity of cholinergic innervation. Alterations of cholinergic markers are comparable in cortical areas in AD, PD, and PD/AD brains. In frontal and temporal cortices, as well as in the hippocampus, choline acetyltransferase activity and binding capacities of M2 and nicotinic binding sites are similarly decreased in these three disorders compared with age-matched control values. M1 receptor binding parameters are not significantly modified in cortical areas in patients with these disorders. In contrast, important differences between AD and PD brain tissues are found in subcortical areas such as the striatum and the thalamus. The density of M1 sites is significantly increased in striatal areas only in patients with AD, whereas densities of nicotinic sites are decreased in thalamus and striatum in PD and PD/AD, but not AD, brain tissues. The binding capacity of M2 sites is apparently unchanged in subcortical areas in all three disorders, although tendencies toward reductions are observed in the striatum of PD and PD/AD patients. Thus, although comparable alterations of various cholinergic markers are observed in cortical areas in the three neurological disorders investigated in the present study, important differences are seen in subcortical areas. This may be relevant to the respective etiological and clinical profiles of AD and PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1729398</PMID><DateCreated><Year>1992</Year><Month>02</Month><Day>13</Day></DateCreated><DateCompleted><Year>1992</Year><Month>02</Month><Day>13</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3042</ISSN><JournalIssue CitedMedium="Print"><Volume>58</Volume><Issue>2</Issue><PubDate><Year>1992</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Journal of neurochemistry</Title><ISOAbbreviation>J. Neurochem.</ISOAbbreviation></Journal><ArticleTitle>Comparative alterations of nicotinic and muscarinic binding sites in Alzheimer's and Parkinson's diseases.</ArticleTitle><Pagination><MedlinePgn>529-41</MedlinePgn></Pagination><Abstract><AbstractText>We have recently reported on the differential alterations of various cholinergic markers in cortical and subcortical regions in Alzheimer's disease (AD). The main purpose of the present study was to determine if cholinergic deficits observed in patients with AD are unique to this disorder or can be generalized to others such as idiopathic Parkinson's disease (PD) and PD with Alzheimer-type dementia (PD/AD). Muscarinic M1, M2, and nicotinic receptor binding parameters (KD and Bmax) were determined in various cortical and subcortical areas using selective radioligands ([3H]pirenzepine, [3H]AF-DX 116, and N[3H]methylcarbamylcholine). Choline acetyltransferase activity was also determined as a marker of the integrity of cholinergic innervation. Alterations of cholinergic markers are comparable in cortical areas in AD, PD, and PD/AD brains. In frontal and temporal cortices, as well as in the hippocampus, choline acetyltransferase activity and binding capacities of M2 and nicotinic binding sites are similarly decreased in these three disorders compared with age-matched control values. M1 receptor binding parameters are not significantly modified in cortical areas in patients with these disorders. In contrast, important differences between AD and PD brain tissues are found in subcortical areas such as the striatum and the thalamus. The density of M1 sites is significantly increased in striatal areas only in patients with AD, whereas densities of nicotinic sites are decreased in thalamus and striatum in PD and PD/AD, but not AD, brain tissues. The binding capacity of M2 sites is apparently unchanged in subcortical areas in all three disorders, although tendencies toward reductions are observed in the striatum of PD and PD/AD patients. Thus, although comparable alterations of various cholinergic markers are observed in cortical areas in the three neurological disorders investigated in the present study, important differences are seen in subcortical areas. This may be relevant to the respective etiological and clinical profiles of AD and PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aubert</LastName><ForeName>I</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Neurology, McGill University, Montreal, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Araujo</LastName><ForeName>D M</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Cécyre</LastName><ForeName>D</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Robitaille</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Gauthier</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Quirion</LastName><ForeName>R</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neurochem</MedlineTA><NlmUniqueID>2985190R</NlmUniqueID><ISSNLinking>0022-3042</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>6M3C89ZY6R</RegistryNumber><NameOfSubstance UI="D009538">Nicotine</NameOfSubstance></Chemical><Chemical><RegistryNumber>7T101UWZ5W</RegistryNumber><NameOfSubstance UI="D009116">Muscarine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.1.6</RegistryNumber><NameOfSubstance UI="D002795">Choline O-Acetyltransferase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001665" MajorTopicYN="N">Binding Sites</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002795" MajorTopicYN="N">Choline O-Acetyltransferase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009116" MajorTopicYN="N">Muscarine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009538" MajorTopicYN="N">Nicotine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1992</Year><Month>2</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1992</Year><Month>2</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1992</Year><Month>2</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1729398</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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