Epidemiology of Parkinson's disease

Kasten, Meike; Chade, Annabel; Tanner, Caroline M.

doi:10.1016/s0072-9752(07)83006-5

Cited by 58 publications

(32 citation statements)

References 251 publications

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“…The population we studied could differ from the general population of PD patients. Nevertheless, considering the age of PD onset and sex distribution, our series resembled the general population of PD 23. The mean severity of PD and the frequency of levodopa-related motor complications in our series are compatible with an average disease duration of 8 years.…”

Section: Discussionsupporting

confidence: 69%

Camptocormia in Parkinson disease: an epidemiological and clinical study

Tiple

Fabbrini

Colosimo

et al. 2009

Journal of Neurology, Neurosurgery & Psychiatry

145

107

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Section: Discussionsupporting

confidence: 69%

Camptocormia in Parkinson disease: an epidemiological and clinical study

Tiple

Fabbrini

Colosimo

et al. 2009

Journal of Neurology, Neurosurgery & Psychiatry

145

107

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“…One such environmental factor has been pesticide exposure (Kasten et al , 2007; Cannon and Greenamyre, 2011), and consistent with these epidemiologic data, animal studies have demonstrated that a number of pesticides may be toxic to dopamine neurons (Richardson et al , 2005). The current study is the first to demonstrate directly the microstructural changes in the SN of human subjects having had chronic, low-dose exposure of a diverse group of pesticides.…”

Section: Discussionmentioning

confidence: 89%

Microstructural changes in the substantia nigra of asymptomatic agricultural workers

Du¹,

Lewis²,

Sterling³

et al. 2014

Neurotoxicology and Teratology

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Parkinson's disease (PD) is marked by the loss of dopamine neurons in the substantia nigra (SN). Although the exact etiology is unknown, sporadic PD is hypothesized to be a result of genetic susceptibility interacting with environmental insult. Epidemiological studies suggest that pesticide exposure is linked to higher PD risk, but there are no studies demonstrating SN changes with chronic pesticide exposure in human subjects. Thus, high resolution T2-weighted magnetic resonance imaging (MRI) and diffusion tensor (DTI) images were obtained from 12 agricultural workers with chronic pesticide exposure, 12 controls, and 12 PD subjects. Neither controls, nor pesticide-exposed subjects, had any parkinsonian symptoms. Exposure history to pesticides was assessed by a structured questionnaire. DTI measures in the SN, including fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD), were obtained for all subjects and compared among groups. Compared to controls, PD patients showed the expected significant changes in all DTI measurements in the SN. The pesticides-exposed subjects, compared to controls, had significantly lower FA values (p=0.022, after multiple comparisons correction), but no significant differences in RD, MD, or AD measures. The study is the first to demonstrate microstructural changes in the SN of human subjects with chronic pesticide exposure. The changes detected by MRI may mark “one of the hits” leading to PD, and underlie the increased risk of PD in pesticide users found in epidemiological studies. Further human studies assisted by these imaging markers may be useful in understanding the etiology of PD.

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“…Idiopathic Parkinson's disease (PD) is the second most common neurodegenerative disorder and the most prevalent type of parkinsonian syndrome (PS) with overall incidence of approximately 17 per 100 000 per year 1 2. Clinical diagnosis is based on presence of fatiguable bradykinesia with one other symptom: tremor, rigidity or postural instability 3 4.…”

Section: Introductionmentioning

confidence: 99%