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Review
. 2024 Jan 20;403(10423):283-292.
doi: 10.1016/S0140-6736(23)01419-8.

The epidemiology of Parkinson's disease

Affiliations
Review

The epidemiology of Parkinson's disease

Yoav Ben-Shlomo et al. Lancet. .

Abstract

The epidemiology of Parkinson's disease shows marked variations in time, geography, ethnicity, age, and sex. Internationally, prevalence has increased over and above demographic changes. There are several potential reasons for this increase, including the decline in other competing causes of death. Whether incidence is increasing, especially in women or in many low-income and middle-income countries where there is a shortage of high-quality data, is less certain. Parkinson's disease is more common in older people and men, and a variety of environmental factors have been suggested to explain why, including exposure to neurotoxic agents. Within countries, there appear to be ethnic differences in disease risk, although these differences might reflect differential access to health care. The cause of Parkinson's disease is multifactorial, and involves genetic and environmental factors. Both risk factors (eg, pesticides) and protective factors (eg, physical activity and tendency to smoke) have been postulated to have a role in Parkinson's disease, although elucidating causality is complicated by the long prodromal period. Following the establishment of public health strategies to prevent cardiovascular diseases and some cancers, chronic neurodegenerative diseases such as Parkinson's disease and dementia are gaining a deserved higher priority. Multipronged prevention strategies are required that tackle population-based primary prevention, high-risk targeted secondary prevention, and Parkinson's disease-modifying therapies for tertiary prevention. Future international collaborations will be required to triangulate evidence from basic, applied, and epidemiological research, thereby enhancing the understanding and prevention of Parkinson's disease at a global level.

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Conflict of interest statement

Declaration of interests YB-S receives grant funding from the Wellcome Trust, Medical Research Council, Healthcare Quality Improvement Partnership, Parkinson's UK, Templeton Foundation, Versus Arthritis, Dunhill Medical Trust, National Institute for Health and Care Research, and the Gatsby Foundation; receives book royalties from Oxford University Press and Wiley books; consulting fees from Human Centric DD; is a member of the Trial Steering Committee for the SIMPLIFIED vitamin D randomised clinical trial in chronic kidney disease patients; and is an unpaid member of the Alzheimer's Society grant board and Alzheimer's Research UK strategy committee. SD is a Dutch Veni Award recipient, and receives funding from Parkinson's UK, Parkinson NL, Davis Phinney Foundation, Edmond J Safra Foundation, Michael J Fox Foundation, Parkinson Vereniging, and Parkinson's Foundation. JL-G receives funding from Michael J Fox Foundation, National Institutes of Health (NIH)/National Institute on Aging (NIA), and Alzheimer's Association Research Fellowship to Promote Diversity (AARFD). CM receives funding from Centogene, Canadian Institutes of Health Research, Michael J Fox Foundation, International Parkinson and Movement Disorders Society, and Parkinson's Foundation; receives consulting fees from Neurocrine; and is a board member of the International Parkinson and Movement Disorders Society. MSL receives research support from the Smart Foundation and grant funding from NIH/National Institute of Neurological Disorders and Stroke (NINDS); has received honoraria from American Academy of Neurology and SUNY Downstate Department of Neurology; has received support from BIOGEN for attending a meeting; and is on the data and safety monitoring board (unpaid) for the NeuroNext/NN10 trial. CT receives grant funding from Parkinson Foundation, Michael J Fox Foundation, Gateway, Roche Genentech, Biogen, NIH/NIA, NIH/NINDS, Department of Defense, Parkinson Study Group, VA Merit, Marcus Program in Precision Medicine, and Bioelectron Technology Corporation; receives consulting fees from CNS Ratings and Grey Matter; has received honoraria from Guidemark Health, American Academy of Neurology, Druker Lecture, Beth Israel Deaconess, Boston, Cynthia L Comella Lecture, Rush University Medical Center, and Tauba Pasik and Pedro Pasik Endowed Lecture in Neurology; has received funding to attend a meeting from Neurocrine; participated on a data and safety monitoring board or advisory board for Acadia, Northwestern University Partners, Harvard University, Neurocrine, Lundbeck, Cadent, Acorda, Adamas, Amneal, Kyowa Kirin, Jazz/Cavion, and Australia Parkinson's Mission; is a committee member for Linked Clinical Trials/Cure Parkinson's Trust, International Parkinson and Movement Disorders Society–Epidemiology Working Group, Telemedicine Working Group, PanAmerican Section Nominating Committee, and American Academy of Neurology–Scientific Plenary Session Topic Committee, Movement Disorders.

Figures

Figure 1:
Figure 1:. Simplified schematic of how risk and protective factors might determine neuropathology and the development of Parkinson’s disease
*While Parkinson’s disease is shown as developing in later life, the age of onset is variable and cases can develop disease at much younger ages.
Figure 2:
Figure 2:. Hypothetical primary, secondary, and tertiary strategies to prevent, slow the onset of, and slow the progression of Parkinson’s disease across the life course
The horizontal line indicates a hypothetical threshold whereby decline in function is sufficiently severe to lead to a clinical diagnosis. (A) Normative trajectory of function that never results in clinical disease. (B) Extended plateau phase; decline is delayed and disease is diagnosed later in life. (C) Normative developmental phase, but rapid decline phase with earlier disease diagnosis. (D) Suboptimal developmental phase (lower plateau) followed by normative decline, leading to earlier disease diagnosis. *No assumptions have been made about the relative effectiveness of each strategy.

Comment in

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