Incidence of Parkinson's disease in Norway: the Norwegian ParkWest study

Alves, Guido; Müller, Bernd; Herlofson, Karen; HogenEsch, Ineke; Telstad, Wenche; Aarsland, Dag; Tysnes, Ole‐Bjørn; Larsen, Jan Petter

doi:10.1136/jnnp.2008.168211

Cited by 240 publications

(225 citation statements)

References 41 publications

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“…Some studies, including our investigation, found a decline in incidence rates for the oldest old,14, 15, 16, 17, 18 and others did not 11, 12, 13. However, varying definitions and small sample sizes make comparisons difficult 1.…”

Section: Discussionmentioning

confidence: 51%

“…Incidence rates are also low for those aged 50‐59 and increase sharply afterward. Age‐specific peaks differ between studies, however, ranging from 80.4 to 678 new cases/100 000 person‐years 11, 12, 13, 14, 15, 16, 17, 18, 19. German data on prevalence and incidence are rare, outdated, and had been designed primarily as door‐to‐door surveys 1.…”

Section: Introductionmentioning

confidence: 99%

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Parkinson's disease in Germany: prevalence and incidence based on health claims data

2016

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BackgroundIn Germany, epidemiological information on Parkinson's disease (PD) is rare and outdated. Considering aging populations, current prevalences and incidence rates about this age‐related disease would be important for adequate public health planning.MethodsWe used newly available health claims data sets from the largest German health insurer dating 2004‐2007 and 2007‐2010 with an analysis population in the base years of 491 038 persons aged 50 and older. Quarter‐specific information about ICD‐10 diagnoses and PD drug prescriptions from the inpatient and outpatient sectors was used to validate PD cases. Estimations were presented for two validation strategies relying on repeated PD diagnoses (SIa) and on one PD diagnosis followed by at least one PD drug prescription (SIb).ResultsThe standardized prevalence was 797 (SIb) to 961/100 000 persons (SIa), showing an age‐specific increase up to category 85‐89 and a decline thereafter. The standardized incidence rate was 192 to 229/100 000 person‐years with a similar age‐specific shape. Prevalences and incidences rates were higher for men compared to women in regard to age.ConclusionsHealth claims data are found to be suitable for PD assessment using the repeated diagnoses or PD drug prescriptions as necessary criteria.

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Section: Discussionmentioning

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Parkinson's disease in Germany: prevalence and incidence based on health claims data

2016

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“…The individuals with PD were obtained from the Norwegian Park West study, a prospective population-based cohort that has been described in detail [2]. Individuals with PD fulfilled the National Institute of Neurological Disorders and Stroke [15] and the UK Parkinson's disease Society Brain Bank [43] diagnostic criteria for the disease at their final visit.…”

Section: Patient Cohorts and Tissue Samplesmentioning

confidence: 99%

Neuronal complex I deficiency occurs throughout the Parkinson’s disease brain, but is not associated with neurodegeneration or mitochondrial DNA damage

et al. 2017

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Mitochondrial complex I deficiency occurs in the substantia nigra of individuals with Parkinson's disease. It is generally believed that this phenomenon is caused by accumulating mitochondrial DNA damage in neurons and that it contributes to the process of neurodegeneration. We hypothesized that if these theories are correct, complex I deficiency should extend beyond the substantia nigra to other affected brain regions in Parkinson's disease and correlate tightly with neuronal mitochondrial DNA damage. To test our hypothesis, we employed a combination of semiquantitative immunohistochemical analyses, Western blot and activity measurements, to assess complex I quantity and function in multiple brain regions from an extensively characterized population-based cohort of idiopathic Parkinson's disease (n = 18) and gender and age matched healthy controls (n = 11). Mitochondrial DNA was assessed in single neurons from the same areas by real-time PCR. Immunohistochemistry showed that neuronal complex I deficiency occurs throughout the Parkinson's disease brain, including areas spared by the neurodegenerative process such as the cerebellum. Activity measurements in brain homogenate confirmed a moderate decrease of complex I function, whereas Western blot was less sensitive, detecting only a mild reduction, which did not reach statistical significance at the group level. With the exception of the substantia nigra, neuronal complex I loss showed no correlation with the load of somatic mitochondrial DNA damage. Interestingly, α-synuclein aggregation was less common in complex I deficient neurons in the substantia nigra. We show that neuronal complex I deficiency is a widespread phenomenon in the Parkinson's disease brain which, contrary to mainstream theory, does not follow the anatomical distribution of neurodegeneration and is not associated with the neuronal load of mitochondrial DNA mutation. Our findings suggest that complex I deficiency in Parkinson's disease can occur independently of mitochondrial DNA damage and may not have a pathogenic role in the neurodegenerative process.

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“…[1]. Bradykinesia or the of stuntment in movements, as main from the list of cardinal symptoms according to Brain Bank Criteria of UK Parkinson's Disease (BBC-UKPCD), was present in all respondents.…”

Section: Discussionmentioning

confidence: 99%