Etiology of Parkinson's disease
Identifieur interne : 003825 ( Main/Curation ); précédent : 003824; suivant : 003826Etiology of Parkinson's disease
Auteurs : A. J. Stoessl [Canada]Source :
- Canadian journal of neurological sciences [ 0317-1671 ] ; 1999.
Descripteurs français
- Pascal (Inist)
- Wicri :
English descriptors
- KwdEn :
- Aging (physiology), Apoptosis (physiology), Environmental factor, Etiology, Free Radicals, Genetics, Human, Humans, Immune System Diseases (complications), Incidence, Infection (complications), Mitochondria (physiology), Nerve Growth Factors (physiology), Parkinson Disease (epidemiology), Parkinson Disease (etiology), Parkinson Disease (genetics), Parkinson disease, Prevalence, Toxin.
- 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.
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Pascal:99-0456202Le document en format XML
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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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