Mechanism of Alzheimer's disease: arguments for a neurotransmitter-aluminium complex implication.
Identifieur interne : 000A68 ( Ncbi/Merge ); précédent : 000A67; suivant : 000A69Mechanism of Alzheimer's disease: arguments for a neurotransmitter-aluminium complex implication.
Auteurs : R. Deloncle [France] ; O. GuillardSource :
- Neurochemical research [ 0364-3190 ] ; 1990.
English descriptors
- KwdEn :
- Aluminum (metabolism), Aluminum (toxicity), Alzheimer Disease (etiology), Alzheimer Disease (metabolism), Alzheimer Disease (physiopathology), Blood-Brain Barrier, Brain (physiopathology), Down Syndrome (physiopathology), Humans, Neurotransmitter Agents (metabolism), Parkinson Disease (physiopathology).
- MESH :
- chemical , metabolism : Aluminum, Neurotransmitter Agents.
- chemical , toxicity : Aluminum.
- etiology : Alzheimer Disease.
- metabolism : Alzheimer Disease.
- physiopathology : Alzheimer Disease, Brain, Down Syndrome, Parkinson Disease.
- Blood-Brain Barrier, Humans.
Abstract
The authors are convinced that in Alzheimer's disease, as in Down's syndrome and Guam-Parkinson dementia, one may find an alteration in blood brain barrier transfer and a resultant imbalance in mineral metabolism. Metals, such as aluminium, which in vivo yield stable complexes with aspartic and glutamic acids act as previously been clearly shown with glutamic acid; they cross the blood brain barrier, and are deposited in the brain. The authors explain how amyloid protein or neurofibrillary tangles could well be produced by aluminium complex formation. Within the brain, in the form precisely of aluminium complex, L-glutamic acid is consequently unable to detoxify ammonia from neurons and to produce L-glutamin. Accumulation of ammonia is subsequently responsible for the neuronal death, affecting each and every neurotransmitter system.
PubMed: 1982955
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 001813
- to stream PubMed, to step Curation: 001772
- to stream PubMed, to step Checkpoint: 001772
Links to Exploration step
pubmed:1982955Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mechanism of Alzheimer's disease: arguments for a neurotransmitter-aluminium complex implication.</title><author><name sortKey="Deloncle, R" sort="Deloncle, R" uniqKey="Deloncle R" first="R" last="Deloncle">R. Deloncle</name><affiliation wicri:level="3"><nlm:affiliation>Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, Tours, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, Tours</wicri:regionArea><placeName><region type="region">Centre-Val de Loire</region><region type="old region">Région Centre</region><settlement type="city">Tours</settlement></placeName></affiliation></author><author><name sortKey="Guillard, O" sort="Guillard, O" uniqKey="Guillard O" first="O" last="Guillard">O. Guillard</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1990">1990</date><idno type="RBID">pubmed:1982955</idno><idno type="pmid">1982955</idno><idno type="wicri:Area/PubMed/Corpus">001813</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001813</idno><idno type="wicri:Area/PubMed/Curation">001772</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001772</idno><idno type="wicri:Area/PubMed/Checkpoint">001772</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001772</idno><idno type="wicri:Area/Ncbi/Merge">000A68</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Mechanism of Alzheimer's disease: arguments for a neurotransmitter-aluminium complex implication.</title><author><name sortKey="Deloncle, R" sort="Deloncle, R" uniqKey="Deloncle R" first="R" last="Deloncle">R. Deloncle</name><affiliation wicri:level="3"><nlm:affiliation>Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, Tours, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, Tours</wicri:regionArea><placeName><region type="region">Centre-Val de Loire</region><region type="old region">Région Centre</region><settlement type="city">Tours</settlement></placeName></affiliation></author><author><name sortKey="Guillard, O" sort="Guillard, O" uniqKey="Guillard O" first="O" last="Guillard">O. Guillard</name></author></analytic><series><title level="j">Neurochemical research</title><idno type="ISSN">0364-3190</idno><imprint><date when="1990" type="published">1990</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aluminum (metabolism)</term><term>Aluminum (toxicity)</term><term>Alzheimer Disease (etiology)</term><term>Alzheimer Disease (metabolism)</term><term>Alzheimer Disease (physiopathology)</term><term>Blood-Brain Barrier</term><term>Brain (physiopathology)</term><term>Down Syndrome (physiopathology)</term><term>Humans</term><term>Neurotransmitter Agents (metabolism)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Aluminum</term><term>Neurotransmitter Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Aluminum</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Alzheimer Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Alzheimer Disease</term><term>Brain</term><term>Down Syndrome</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Blood-Brain Barrier</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The authors are convinced that in Alzheimer's disease, as in Down's syndrome and Guam-Parkinson dementia, one may find an alteration in blood brain barrier transfer and a resultant imbalance in mineral metabolism. Metals, such as aluminium, which in vivo yield stable complexes with aspartic and glutamic acids act as previously been clearly shown with glutamic acid; they cross the blood brain barrier, and are deposited in the brain. The authors explain how amyloid protein or neurofibrillary tangles could well be produced by aluminium complex formation. Within the brain, in the form precisely of aluminium complex, L-glutamic acid is consequently unable to detoxify ammonia from neurons and to produce L-glutamin. Accumulation of ammonia is subsequently responsible for the neuronal death, affecting each and every neurotransmitter system.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1982955</PMID><DateCreated><Year>1991</Year><Month>07</Month><Day>23</Day></DateCreated><DateCompleted><Year>1991</Year><Month>07</Month><Day>23</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0364-3190</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><Issue>12</Issue><PubDate><Year>1990</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Neurochemical research</Title><ISOAbbreviation>Neurochem. Res.</ISOAbbreviation></Journal><ArticleTitle>Mechanism of Alzheimer's disease: arguments for a neurotransmitter-aluminium complex implication.</ArticleTitle><Pagination><MedlinePgn>1239-45</MedlinePgn></Pagination><Abstract><AbstractText>The authors are convinced that in Alzheimer's disease, as in Down's syndrome and Guam-Parkinson dementia, one may find an alteration in blood brain barrier transfer and a resultant imbalance in mineral metabolism. Metals, such as aluminium, which in vivo yield stable complexes with aspartic and glutamic acids act as previously been clearly shown with glutamic acid; they cross the blood brain barrier, and are deposited in the brain. The authors explain how amyloid protein or neurofibrillary tangles could well be produced by aluminium complex formation. Within the brain, in the form precisely of aluminium complex, L-glutamic acid is consequently unable to detoxify ammonia from neurons and to produce L-glutamin. Accumulation of ammonia is subsequently responsible for the neuronal death, affecting each and every neurotransmitter system.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Deloncle</LastName><ForeName>R</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, Tours, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guillard</LastName><ForeName>O</ForeName><Initials>O</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurochem Res</MedlineTA><NlmUniqueID>7613461</NlmUniqueID><ISSNLinking>0364-3190</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018377">Neurotransmitter Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>CPD4NFA903</RegistryNumber><NameOfSubstance UI="D000535">Aluminum</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000535" MajorTopicYN="N">Aluminum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001812" MajorTopicYN="Y">Blood-Brain Barrier</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004314" MajorTopicYN="N">Down Syndrome</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018377" MajorTopicYN="N">Neurotransmitter Agents</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>85</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1990</Year><Month>12</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1990</Year><Month>12</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1990</Year><Month>12</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1982955</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Centre-Val de Loire</li><li>Région Centre</li></region><settlement><li>Tours</li></settlement></list><tree><noCountry><name sortKey="Guillard, O" sort="Guillard, O" uniqKey="Guillard O" first="O" last="Guillard">O. Guillard</name></noCountry><country name="France"><region name="Centre-Val de Loire"><name sortKey="Deloncle, R" sort="Deloncle, R" uniqKey="Deloncle R" first="R" last="Deloncle">R. Deloncle</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/Ncbi/Merge
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000A68 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd -nk 000A68 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= Ncbi
|étape= Merge
|type= RBID
|clé= pubmed:1982955
|texte= Mechanism of Alzheimer's disease: arguments for a neurotransmitter-aluminium complex implication.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/RBID.i -Sk "pubmed:1982955" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |