Etiology of Parkinson's disease.
Identifieur interne : 001694 ( PubMed/Corpus ); précédent : 001693; suivant : 001695Etiology of Parkinson's disease.
Auteurs : A J StoesslSource :
- The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques [ 0317-1671 ] ; 1999.
English descriptors
- KwdEn :
- Aging (physiology), Apoptosis (physiology), Free Radicals, Humans, Immune System Diseases (complications), Incidence, Infection (complications), Mitochondria (physiology), Nerve Growth Factors (physiology), Parkinson Disease (epidemiology), Parkinson Disease (etiology), Parkinson Disease (genetics), Prevalence.
- MESH :
- chemical , physiology : Nerve Growth Factors.
- chemical : Free Radicals.
- complications : Immune System Diseases, Infection.
- epidemiology : Parkinson Disease.
- etiology : Parkinson Disease.
- genetics : Parkinson Disease.
- physiology : Aging, Apoptosis, Mitochondria.
- Humans, Incidence, Prevalence.
Abstract
Controversy over the etiology and pathogenesis of Parkinson's disease (PD) has continued for many years and while the details have changed, the uncertainty persists. Although heritability was most emphatically refuted a decade ago by many investigators, recent progress firmly indicates that genetic factors at least play a role, although probably to a variable degree from one individual to another. Evidence for a variety of other etiological factors is amassed from epidemiological studies, animal models, molecular and cellular biology. Genetic factors, infectious and immunological abnormalities, the effects of ageing, toxins (endogenous as well as exogenous) and other environmental factors may all contribute to the development of PD. Loss of nigral dopaminergic neurons may be mediated by varying combinations of oxidative free radical toxicity, impaired mitochondrial function, "weak excitotoxicity" and abnormal handling of cytoskeletal proteins, all of which may shift the balance regulating apoptotic cell death.
PubMed: 10451754
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pubmed:10451754Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (physiology)</term>
<term>Apoptosis (physiology)</term>
<term>Free Radicals</term>
<term>Humans</term>
<term>Immune System Diseases (complications)</term>
<term>Incidence</term>
<term>Infection (complications)</term>
<term>Mitochondria (physiology)</term>
<term>Nerve Growth Factors (physiology)</term>
<term>Parkinson Disease (epidemiology)</term>
<term>Parkinson Disease (etiology)</term>
<term>Parkinson Disease (genetics)</term>
<term>Prevalence</term>
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<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Nerve Growth Factors</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Aging</term>
<term>Apoptosis</term>
<term>Mitochondria</term>
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<front><div type="abstract" xml:lang="en">Controversy over the etiology and pathogenesis of Parkinson's disease (PD) has continued for many years and while the details have changed, the uncertainty persists. Although heritability was most emphatically refuted a decade ago by many investigators, recent progress firmly indicates that genetic factors at least play a role, although probably to a variable degree from one individual to another. Evidence for a variety of other etiological factors is amassed from epidemiological studies, animal models, molecular and cellular biology. Genetic factors, infectious and immunological abnormalities, the effects of ageing, toxins (endogenous as well as exogenous) and other environmental factors may all contribute to the development of PD. Loss of nigral dopaminergic neurons may be mediated by varying combinations of oxidative free radical toxicity, impaired mitochondrial function, "weak excitotoxicity" and abnormal handling of cytoskeletal proteins, all of which may shift the balance regulating apoptotic cell death.</div>
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<Title>The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques</Title>
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<Abstract><AbstractText>Controversy over the etiology and pathogenesis of Parkinson's disease (PD) has continued for many years and while the details have changed, the uncertainty persists. Although heritability was most emphatically refuted a decade ago by many investigators, recent progress firmly indicates that genetic factors at least play a role, although probably to a variable degree from one individual to another. Evidence for a variety of other etiological factors is amassed from epidemiological studies, animal models, molecular and cellular biology. Genetic factors, infectious and immunological abnormalities, the effects of ageing, toxins (endogenous as well as exogenous) and other environmental factors may all contribute to the development of PD. Loss of nigral dopaminergic neurons may be mediated by varying combinations of oxidative free radical toxicity, impaired mitochondrial function, "weak excitotoxicity" and abnormal handling of cytoskeletal proteins, all of which may shift the balance regulating apoptotic cell death.</AbstractText>
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<NumberOfReferences>117</NumberOfReferences>
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