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1.
Neuroepidemiology ; 28(4): 193-6, 2007.
Artículo en Inglés | MEDLINE | ID: mdl-17851257

RESUMEN

BACKGROUND: Several lines of evidence suggest a role of inflammatory processes in Parkinson disease, although it is still unclear whether inflammation is a cause or rather a consequence of neurodegeneration. METHODS: In a prospective population-based cohort study among 6,512 participants aged >or=55 years, with repeated in-person examination, we evaluated the association between cumulative use of nonsteroidal anti-inflammatory drugs (NSAIDs) and the risk of Parkinson disease. Complete information on filled prescriptions was available from automated pharmacy records. Data were analyzed by means of Cox proportional hazards regression analysis, adjusted for age, sex, smoking habits and coffee consumption. RESULTS: After an average 9.4 years of follow-up, 88 new cases of Parkinson disease were detected. No association was found between use of NSAIDs and the risk of Parkinson disease (adjusted hazard ratio for any NSAID use, 1.50; 95% confidence interval, 0.95-2.37). CONCLUSION: Our findings do not support the hypothesis that NSAIDs might decrease the risk of Parkinson disease.


Asunto(s)
Antiinflamatorios no Esteroideos/uso terapéutico , Enfermedad de Parkinson/epidemiología , Anciano , Antiinflamatorios no Esteroideos/efectos adversos , Aspirina/efectos adversos , Aspirina/uso terapéutico , Estudios de Cohortes , Inhibidores de la Ciclooxigenasa/efectos adversos , Inhibidores de la Ciclooxigenasa/uso terapéutico , Femenino , Humanos , Masculino , Persona de Mediana Edad , Enfermedad de Parkinson/prevención & control , Estudios Prospectivos , Factores de Riesgo
3.
Neurobiol Dis ; 14(3): 619-23, 2003 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-14678776

RESUMEN

Hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D) is a rare autosomal dominant disorder caused by an amyloid-beta precursor protein (AbetaPP) 693 mutation that clinically leads to recurrent hemorrhagic strokes and dementia. The disease is pathologically characterised by the deposition of Abeta in cerebral blood vessels and as plaques in the brain parenchyma. This study measured the Abeta40 and Abeta42 concentration in plasma of Dutch AbetaPP693 mutation carriers and controls. We found that the Abeta40 concentration was not different between AbetaPP693 mutation carriers and controls. However, the Abeta42 concentration was significantly decreased in the mutation carriers. No correlation exists between the APOE(epsilon)4 allele and the plasma of Abeta40 and Abeta42 levels in HCHWA-D patients. This finding contrasted with the increased concentrations found in Alzheimer's disease. Therefore it is suggested that the Dutch AbetaPP693 mutation located within the Abeta coding region of the AbetaPP gene has a different effect not only on clinical and pathological expression but also on Abeta processing.


Asunto(s)
Péptidos beta-Amiloides/sangre , Angiopatía Amiloide Cerebral Familiar/sangre , Angiopatía Amiloide Cerebral Familiar/genética , Regulación hacia Abajo/genética , Fragmentos de Péptidos/sangre , Adulto , Anciano , Apolipoproteína E4 , Apolipoproteínas E/metabolismo , Encéfalo/irrigación sanguínea , Encéfalo/metabolismo , Encéfalo/patología , Arterias Cerebrales/metabolismo , Arterias Cerebrales/patología , Arterias Cerebrales/fisiopatología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Mutación/genética
5.
Radiology ; 224(3): 791-6, 2002 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-12202716

RESUMEN

PURPOSE: To assess the prevalence and distribution of subcortical lacunar lesions (SLLs) in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), to determine whether SLLs are an abnormal finding by studying their prevalence in healthy subjects, and to assess whether SLLs occur in other conditions associated with small vessel disease and white matter areas of high signal intensity (WMH). MATERIALS AND METHODS: The presence of SLLs, their location, and their relation to other abnormalities were assessed on magnetic resonance (MR) images (T1-weighted, T2-weighted, and fluid-attenuated inversion-recovery) obtained in 34 CADASIL patients and 20 healthy family members. Three additional control groups of healthy volunteers, elderly patients with vascular risk factors, and patients with another hereditary small vessel disease were also screened for the presence and location of SLLs. Sensitivity and specificity of the presence of SLLs for the diagnosis of CADASIL were assessed. RESULTS: SLLs were found in 20 (59%) of CADASIL patients. Incidence of SLLs increased with age (20%, <30 years; 50%, 30-50 years; 80%, >50 years). SLLs invariably occurred in the anterior temporal lobes and in areas where diffuse WMH expanded into arcuate fibers. From the anterior temporal lobe, the lesions could extend dorsally into the temporal lobes and rostrally into the frontal lobes. Lesions were not found in the parietal and occipital lobes. None of the control subjects had SLLs. Specificity and sensitivity of SLLs for CADASIL were 100% and 59%, respectively. CONCLUSION: SLLs are an abnormal finding at MR imaging that frequently occur in CADASIL patients.


Asunto(s)
Enfermedades Arteriales Cerebrales/diagnóstico por imagen , Enfermedades Arteriales Cerebrales/genética , Infarto Cerebral/complicaciones , Demencia Vascular/complicaciones , Imagen por Resonancia Magnética , Adulto , Anciano , Encéfalo/diagnóstico por imagen , Enfermedades Arteriales Cerebrales/congénito , Infarto Cerebral/diagnóstico por imagen , Demencia Vascular/diagnóstico por imagen , Femenino , Genes Dominantes , Humanos , Masculino , Persona de Mediana Edad , Radiografía , Sensibilidad y Especificidad
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