Toward a molecular neuropsychiatry of neurodegenerative diseases
Identifieur interne : 001689 ( Main/Exploration ); précédent : 001688; suivant : 001690Toward a molecular neuropsychiatry of neurodegenerative diseases
Auteurs : Jeffrey L. Cummings [États-Unis]Source :
- Annals of Neurology [ 0364-5134 ] ; 2003-08.
Abstract
Quantitative neuropsychiatry has provided increasingly precise descriptions of behavioral phenotypes associated with neurodegenerative disorders. Degenerative diseases of the brain are disturbances of protein metabolism, with failure of protein degredation by the ubiquitin‐proteosome system, production of neurotoxic peptide oligomers, and accumulation of intracellular protein deposits. Abnormalities of amyloid beta peptide, alpha‐synuclein protein, and hyperphosphorylated tau protein account for more than 90% of degenerative dementias. Functionally related neuroanatomical systems have shared metabolic characteristics and common vulnerabilities to protein dysmetabolism, providing the basis for phenotypes that reflect the underlying proteotype. Patients with alpha‐synuclein disorders are particularly prone to hallucinations, delusions, and rapid eye movement sleep behavior disorder. Patients with tauopathies manifest disproportionate disinhibition and apathy, and may exhibit compulsions. Alzheimer's disease is a triple proteinopathy with abnormalities of A‐beta, tau, and alpha‐synculein leading to a complex behavioral phenotype. This molecular approach to neuropsychiatry may assist in understanding the mechanisms of degenerative diseases, provide insight into the pathophysiology of neuropsychiatric symptoms, and contribute to monitoring disease‐modifying therapies. Ann Neurol 2003
Url:
DOI: 10.1002/ana.10616
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Toward a molecular neuropsychiatry of neurodegenerative diseases</title><author><name sortKey="Cummings, Jeffrey L" sort="Cummings, Jeffrey L" uniqKey="Cummings J" first="Jeffrey L." last="Cummings">Jeffrey L. Cummings</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:55EFE62F637981E939E60C108AA4F981A0860301</idno><date when="2003" year="2003">2003</date><idno type="doi">10.1002/ana.10616</idno><idno type="url">https://api.istex.fr/document/55EFE62F637981E939E60C108AA4F981A0860301/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000F61</idno><idno type="wicri:Area/Main/Curation">000D79</idno><idno type="wicri:Area/Main/Exploration">001689</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Toward a molecular neuropsychiatry of neurodegenerative diseases</title><author><name sortKey="Cummings, Jeffrey L" sort="Cummings, Jeffrey L" uniqKey="Cummings J" first="Jeffrey L." last="Cummings">Jeffrey L. Cummings</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Departments of Neurology and Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</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="2003-08">2003-08</date><biblScope unit="volume">54</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="147">147</biblScope><biblScope unit="page" to="154">154</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">55EFE62F637981E939E60C108AA4F981A0860301</idno><idno type="DOI">10.1002/ana.10616</idno><idno type="ArticleID">ANA10616</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">Quantitative neuropsychiatry has provided increasingly precise descriptions of behavioral phenotypes associated with neurodegenerative disorders. Degenerative diseases of the brain are disturbances of protein metabolism, with failure of protein degredation by the ubiquitin‐proteosome system, production of neurotoxic peptide oligomers, and accumulation of intracellular protein deposits. Abnormalities of amyloid beta peptide, alpha‐synuclein protein, and hyperphosphorylated tau protein account for more than 90% of degenerative dementias. Functionally related neuroanatomical systems have shared metabolic characteristics and common vulnerabilities to protein dysmetabolism, providing the basis for phenotypes that reflect the underlying proteotype. Patients with alpha‐synuclein disorders are particularly prone to hallucinations, delusions, and rapid eye movement sleep behavior disorder. Patients with tauopathies manifest disproportionate disinhibition and apathy, and may exhibit compulsions. Alzheimer's disease is a triple proteinopathy with abnormalities of A‐beta, tau, and alpha‐synculein leading to a complex behavioral phenotype. This molecular approach to neuropsychiatry may assist in understanding the mechanisms of degenerative diseases, provide insight into the pathophysiology of neuropsychiatric symptoms, and contribute to monitoring disease‐modifying therapies. Ann Neurol 2003</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Cummings, Jeffrey L" sort="Cummings, Jeffrey L" uniqKey="Cummings J" first="Jeffrey L." last="Cummings">Jeffrey L. Cummings</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001689 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001689 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:55EFE62F637981E939E60C108AA4F981A0860301
|texte= Toward a molecular neuropsychiatry of neurodegenerative diseases
}}
| This area was generated with Dilib version V0.6.23. |  |