Neurochemical deficits in pathological brain aging: specificity and possible relevance for treatment strategies.
Identifieur interne : 001A80 ( PubMed/Checkpoint ); précédent : 001A79; suivant : 001A81Neurochemical deficits in pathological brain aging: specificity and possible relevance for treatment strategies.
Auteurs : R. Quirion [Canada] ; I. Aubert ; Y. Robitaille ; S. Gauthier ; D M Araujo ; J G ChabotSource :
- Clinical neuropharmacology [ 0362-5664 ] ; 1990.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Choline O-Acetyltransferase.
- metabolism : Aging, Alzheimer Disease, Parkinson Disease.
- physiology : Brain Chemistry, Receptors, Cholinergic, Synapses.
- therapy : Alzheimer Disease.
- Animals, Humans.
Abstract
Normal brain aging is accompanied by the losses of certain neuronal populations and the appearance of structures such as neuronal plaques and neurofibrillary tangles. Additionally, various neurotransmitter systems are altered in the elderly, although marked variations are observed between individuals, suggesting important differences between successful and unsuccessful aging. In certain pathological conditions, only certain features of normal aging are exacerbated. For example, the densities of forebrain cholinergic neurons are markedly decreased in cortical and hippocampal (but not striatal) areas in Alzheimer's disease. We discuss here the comparative alterations of cholinergic markers in certain neurological disorders such as Alzheimer's disease, Parkinson's disease, and the combined pathology. Differential alterations of brain cholinergic profile are observed in each disorder, this most likely having functional significance. We also found that muscarinic receptors of the M2 subtype act as negative autoreceptors to decrease brain acetylcholine release, whereas nicotinic agonists induced the opposite effect. This suggests that blockade of negative M2 or stimulation of positive nicotinic autoreceptors could have beneficial effects in Alzheimer's disease. Additionally, modulation of heteroreceptor activation such as the serotonergic or interleukin-2 sites located on or in proximity to cholinergic nerve terminals could offer alternate strategies for the treatment of cholinergic deficits in pathological brain aging.
PubMed: 2093419
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:2093419Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neurochemical deficits in pathological brain aging: specificity and possible relevance for treatment strategies.</title><author><name sortKey="Quirion, R" sort="Quirion, R" uniqKey="Quirion R" first="R" last="Quirion">R. Quirion</name><affiliation wicri:level="4"><nlm:affiliation>Douglas Hospital Research Centre, McGill University, Verdun, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Douglas Hospital Research Centre, McGill University, Verdun, Quebec</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Aubert, I" sort="Aubert, I" uniqKey="Aubert I" first="I" last="Aubert">I. Aubert</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="Araujo, D M" sort="Araujo, D M" uniqKey="Araujo D" first="D M" last="Araujo">D M Araujo</name></author><author><name sortKey="Chabot, J G" sort="Chabot, J G" uniqKey="Chabot J" first="J G" last="Chabot">J G Chabot</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1990">1990</date><idno type="RBID">pubmed:2093419</idno><idno type="pmid">2093419</idno><idno type="wicri:Area/PubMed/Corpus">001B92</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001B92</idno><idno type="wicri:Area/PubMed/Curation">001B92</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001B92</idno><idno type="wicri:Area/PubMed/Checkpoint">001B92</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001B92</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neurochemical deficits in pathological brain aging: specificity and possible relevance for treatment strategies.</title><author><name sortKey="Quirion, R" sort="Quirion, R" uniqKey="Quirion R" first="R" last="Quirion">R. Quirion</name><affiliation wicri:level="4"><nlm:affiliation>Douglas Hospital Research Centre, McGill University, Verdun, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Douglas Hospital Research Centre, McGill University, Verdun, Quebec</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Aubert, I" sort="Aubert, I" uniqKey="Aubert I" first="I" last="Aubert">I. Aubert</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="Araujo, D M" sort="Araujo, D M" uniqKey="Araujo D" first="D M" last="Araujo">D M Araujo</name></author><author><name sortKey="Chabot, J G" sort="Chabot, J G" uniqKey="Chabot J" first="J G" last="Chabot">J G Chabot</name></author></analytic><series><title level="j">Clinical neuropharmacology</title><idno type="ISSN">0362-5664</idno><imprint><date when="1990" type="published">1990</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (metabolism)</term><term>Alzheimer Disease (metabolism)</term><term>Alzheimer Disease (therapy)</term><term>Animals</term><term>Brain Chemistry (physiology)</term><term>Choline O-Acetyltransferase (metabolism)</term><term>Humans</term><term>Parkinson Disease (metabolism)</term><term>Receptors, Cholinergic (physiology)</term><term>Synapses (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Choline O-Acetyltransferase</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aging</term><term>Alzheimer Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Brain Chemistry</term><term>Receptors, Cholinergic</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Alzheimer Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Normal brain aging is accompanied by the losses of certain neuronal populations and the appearance of structures such as neuronal plaques and neurofibrillary tangles. Additionally, various neurotransmitter systems are altered in the elderly, although marked variations are observed between individuals, suggesting important differences between successful and unsuccessful aging. In certain pathological conditions, only certain features of normal aging are exacerbated. For example, the densities of forebrain cholinergic neurons are markedly decreased in cortical and hippocampal (but not striatal) areas in Alzheimer's disease. We discuss here the comparative alterations of cholinergic markers in certain neurological disorders such as Alzheimer's disease, Parkinson's disease, and the combined pathology. Differential alterations of brain cholinergic profile are observed in each disorder, this most likely having functional significance. We also found that muscarinic receptors of the M2 subtype act as negative autoreceptors to decrease brain acetylcholine release, whereas nicotinic agonists induced the opposite effect. This suggests that blockade of negative M2 or stimulation of positive nicotinic autoreceptors could have beneficial effects in Alzheimer's disease. Additionally, modulation of heteroreceptor activation such as the serotonergic or interleukin-2 sites located on or in proximity to cholinergic nerve terminals could offer alternate strategies for the treatment of cholinergic deficits in pathological brain aging.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2093419</PMID><DateCreated><Year>1991</Year><Month>06</Month><Day>21</Day></DateCreated><DateCompleted><Year>1991</Year><Month>06</Month><Day>21</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0362-5664</ISSN><JournalIssue CitedMedium="Print"><Volume>13 Suppl 3</Volume><PubDate><Year>1990</Year></PubDate></JournalIssue><Title>Clinical neuropharmacology</Title><ISOAbbreviation>Clin Neuropharmacol</ISOAbbreviation></Journal><ArticleTitle>Neurochemical deficits in pathological brain aging: specificity and possible relevance for treatment strategies.</ArticleTitle><Pagination><MedlinePgn>S73-80</MedlinePgn></Pagination><Abstract><AbstractText>Normal brain aging is accompanied by the losses of certain neuronal populations and the appearance of structures such as neuronal plaques and neurofibrillary tangles. Additionally, various neurotransmitter systems are altered in the elderly, although marked variations are observed between individuals, suggesting important differences between successful and unsuccessful aging. In certain pathological conditions, only certain features of normal aging are exacerbated. For example, the densities of forebrain cholinergic neurons are markedly decreased in cortical and hippocampal (but not striatal) areas in Alzheimer's disease. We discuss here the comparative alterations of cholinergic markers in certain neurological disorders such as Alzheimer's disease, Parkinson's disease, and the combined pathology. Differential alterations of brain cholinergic profile are observed in each disorder, this most likely having functional significance. We also found that muscarinic receptors of the M2 subtype act as negative autoreceptors to decrease brain acetylcholine release, whereas nicotinic agonists induced the opposite effect. This suggests that blockade of negative M2 or stimulation of positive nicotinic autoreceptors could have beneficial effects in Alzheimer's disease. Additionally, modulation of heteroreceptor activation such as the serotonergic or interleukin-2 sites located on or in proximity to cholinergic nerve terminals could offer alternate strategies for the treatment of cholinergic deficits in pathological brain aging.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Quirion</LastName><ForeName>R</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Douglas Hospital Research Centre, McGill University, Verdun, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aubert</LastName><ForeName>I</ForeName><Initials>I</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>Araujo</LastName><ForeName>D M</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Chabot</LastName><ForeName>J G</ForeName><Initials>JG</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Neuropharmacol</MedlineTA><NlmUniqueID>7607910</NlmUniqueID><ISSNLinking>0362-5664</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011950">Receptors, Cholinergic</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="D000375" MajorTopicYN="N">Aging</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001923" MajorTopicYN="N">Brain Chemistry</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002795" MajorTopicYN="N">Choline O-Acetyltransferase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011950" MajorTopicYN="N">Receptors, Cholinergic</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013569" MajorTopicYN="N">Synapses</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>36</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1990</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1990</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1990</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2093419</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country><region><li>Québec</li></region><settlement><li>Montréal</li></settlement><orgName><li>Université McGill</li></orgName></list><tree><noCountry><name sortKey="Araujo, D M" sort="Araujo, D M" uniqKey="Araujo D" first="D M" last="Araujo">D M Araujo</name><name sortKey="Aubert, I" sort="Aubert, I" uniqKey="Aubert I" first="I" last="Aubert">I. Aubert</name><name sortKey="Chabot, J G" sort="Chabot, J G" uniqKey="Chabot J" first="J G" last="Chabot">J G Chabot</name><name sortKey="Gauthier, S" sort="Gauthier, S" uniqKey="Gauthier S" first="S" last="Gauthier">S. Gauthier</name><name sortKey="Robitaille, Y" sort="Robitaille, Y" uniqKey="Robitaille Y" first="Y" last="Robitaille">Y. Robitaille</name></noCountry><country name="Canada"><region name="Québec"><name sortKey="Quirion, R" sort="Quirion, R" uniqKey="Quirion R" first="R" last="Quirion">R. Quirion</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PubMed/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001A80 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 001A80 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Canada
|area= ParkinsonCanadaV1
|flux= PubMed
|étape= Checkpoint
|type= RBID
|clé= pubmed:2093419
|texte= Neurochemical deficits in pathological brain aging: specificity and possible relevance for treatment strategies.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i -Sk "pubmed:2093419" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonCanadaV1
| This area was generated with Dilib version V0.6.29. |  |