Meeting Report: Consensus Statement—Parkinson’s Disease and the Environment: Collaborative on Health and the Environment and Parkinson’s Action Network (CHE PAN) Conference 26–28 June 2007

Bronstein, Jeff M.; Carvey, Paul M.; Chen, Honglei; Cory‐Slechta, Deborah A.; Monte, Donato A. Di; Duda, John E.; English, Paul; Goldman, Samuel; Grate, Stephen J.; Hansen, Johnni; Hoppin, Jane A.; Jewell, Sarah A.; Kamel, Freya; Koroshetz, Walter J.; Langston, J. William; Logroscino, Giancarlo; Nelson, Lorene M.; Ravina, Bernard; Rocca, Walter A.; Ross, G. Webster; Schettler, Ted; Schwarzschild, Michael A.; Scott, Bill; Seegal, Richard F.; Singleton, Andrew; Steenland, Kyle; Tanner, Caroline M.; Eeden, Stephen Van Den; Weisskopf, Marc G.

doi:10.1289/ehp.11702

Cited by 69 publications

(56 citation statements)

References 80 publications

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“…classification of strength of evidence, also applied in a recent consensus statement regarding environmental risk factors in PD [667]. There is substantial evidence that smoking is protective and coffee could be protective against PD, but the physiologic mechanisms for these relations are poorly understood.…”

Section: Comments and Perspectivesmentioning

confidence: 99%

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Epidemiology and etiology of Parkinson’s disease: a review of the evidence

et al. 2011

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Section: Comments and Perspectivesmentioning

confidence: 99%

“…Such an intervention is obviously complicated by the trade-off between possible beneficial effects on PD and adverse effects in terms of risk of gout. [667]. The categories are described as follows: 1.…”

Section: Comments and Perspectivesmentioning

confidence: 99%

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

et al. 2011

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“…The rise in the incidence of autism dramatically exceeded the simultaneous increase in population growth in the longitudinal study by Cavagnaro (2009). The role of unidentified environmental stressors in neurodegenerative disorders has been repeatedly implicated in several reports (Altevogt, Hanson, and Leshner 2008;Bronstein et al 2009;Mayeux 2004). Less than 5% of disease incidence is due to a single gene mutation alone (Willett 2002).…”

Section: Supporting Rationalementioning

confidence: 99%

Histopathological Evaluation of the Nervous System in National Toxicology Program Rodent Studies

et al. 2011

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This article outlines the changes and underlying rationale for modifications to the histopathological evaluation of the nervous system during toxicology and carcinogenesis studies conducted by the National Toxicology Program (NTP). In the past, routine evaluation of the nervous system was mostly limited to three sections of brain, and occasionally the spinal cord and peripheral nerves. Factors such as the increasing occurrence of human neurological diseases and associated economical cost burden, the role of unidentified environmental stressors in neurodegenerative disorders, multiple therapeutic drug-induced neuropathies noted in human clinical trials, and the exponential use of environmental chemicals with unknown neurotoxic potential necessitate a more extensive evaluation of the nervous system. The NTP has modified its protocol to include examination of key anatomic subsites related to neurodegenerative diseases such as Parkinson's disease. Modifications include four additional sections of the brain. Increasing the number of brain sections permits examination of a greater number of specific anatomic subsites with unique vulnerability. In addition, the spinal cord, peripheral nerves, trigeminal ganglion, and intestinal autonomic ganglia will be evaluated as needed. It is expected that this modified approach will increase the sensitivity of detecting neurotoxicants and neurocarcinogens important in human neurologic and neurodegenerative disorders.Keywords: neuropathology; histopathology; brain; nervous system; NTP; nervous system; screening.Since its inception in 1978, one of the major goals of the National Toxicology Program (NTP) has been to identify carcinogens (based on carcinogenicity for laboratory animals under conditions of study as adopted by NTP since 1983) based on 2-year rodent bioassays. The standard three sections of the brain examined in such routine studies were taken at the levels of (1) the basal ganglia, including the cerebrum at the frontal cortical level; (2) the thalamus at the mid-infundibular level; and (3) a mid-cerebellar section that included the cerebellum and medulla. For studies in which clinical neurological signs were noted, or studies in which agents were suspected to be neurotoxic, sections of the spinal cord and the sciatic nerve were also examined. In addition to the identification of carcinogens, the NTP has recently started a number of initiatives to assess adverse, nonneoplastic toxicological effects. Since environmental factors that affect nonneoplastic conditions such as immune-mediated diseases (Virgolini et al. 2005) and reproductive disorders (Davey et al. 2008) are increasingly common, initiatives within the NTP have included enhanced immunopathology as well as revised criteria for histopathological evaluation in reproductive and developmental toxicity studies. Similarly, increasing attention to the role of environmental factors in neurological disorders such as Parkinson's disease ) and autism (Cavagnaro 2007) also emphasizes the need for improved toxicity e...

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“…This view has now dramatically changed. Even though the role of accidental risk factors (e.g., traumatic brain injury) or environmental factors (e.g., exposure to agricultural pesticides or industrial solvents) is increasingly documented [9], it is clear that these environmental factors act in concert with genetic risk factors [10,11]. Furthermore, the identification of several mutations that cause familial forms of PD has revealed mechanisms shared by these rare disease forms and the much more common sporadic forms.…”

Section: Introductionmentioning

confidence: 99%

A Progressive Mouse Model of Parkinson's Disease: The Thy1-aSyn (“Line 61”) Mice

et al. 2012

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Identification of mutations that cause rare familial forms of Parkinson's disease (PD) and subsequent studies of genetic risk factors for sporadic PD have led to an improved understanding of the pathological mechanisms that may cause nonfamilial PD. In particular, genetic and pathological studies strongly suggest that alpha-synuclein, albeit very rarely mutated in PD patients, plays a critical role in the vast majority of individuals with the sporadic form of the disease. We have extensively characterized a mouse model over-expressing full-length, human, wild-type alpha-synuclein under the Thy-1 promoter. We have also shown that this model reproduces many features of sporadic PD, including progressive changes in dopamine release and striatal content, alphasynuclein pathology, deficits in motor and nonmotor functions that are affected in pre-manifest and manifest phases of PD, inflammation, and biochemical and molecular changes similar to those observed in PD. Preclinical studies have already demonstrated improvement with promising new drugs in this model, which provides an opportunity to test novel neuroprotective strategies during different phases of the disorder using endpoint measures with high power to detect drug effects.

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Meeting Report: Consensus Statement—Parkinson’s Disease and the Environment: Collaborative on Health and the Environment and Parkinson’s Action Network (CHE PAN) Conference 26–28 June 2007

Cited by 69 publications

References 80 publications

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

Histopathological Evaluation of the Nervous System in National Toxicology Program Rodent Studies

A Progressive Mouse Model of Parkinson's Disease: The Thy1-aSyn (“Line 61”) Mice

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