The epidemiology of Parkinson's disease (PD) shows significant variations in time, geography, ethnicity, age, and sex. Prevalence has increased globally, partly due to reduced competing causes of death. Incidence is less certain, especially in low- and middle-income countries. PD is more common in older adults and men, with environmental factors like exposure to neurotoxins contributing to risk. Ethnic differences in disease risk exist, though they may reflect healthcare access disparities. PD is multifactorial, involving both genetic and environmental factors. Risk factors (e.g., pesticides) and protective factors (e.g., physical activity) are implicated, though causality is complex due to the long prodromal period. Public health strategies are needed for primary, secondary, and tertiary prevention. International collaboration is essential to enhance understanding and prevention of PD globally. PD diagnosis is based on clinical features, with biomarkers being explored for preclinical detection. Genetic factors, such as mutations in LRRK2, CHCHD2, VPS35, SNCA, PARKIN, DJ1, and PINK1, are associated with monogenic forms. The UK Brain Bank and MDS criteria are widely used for diagnosis. Diagnostic accuracy varies, and biomarker assays may help distinguish PD from other parkinsonian syndromes. Epidemiological studies show increasing prevalence, particularly in low- and middle-income countries, linked to longevity and environmental factors. Age is a key risk factor, with higher undiagnosed cases in older adults. Men have a higher incidence and mortality risk than women, though the exact reasons are unclear. Socioeconomic status is associated with disease risk, with lower status individuals facing greater exposure to neurotoxins. Determinants of PD include environmental toxins (pesticides, solvents, air pollution), lifestyle factors (diet, physical activity, smoking), and genetic predisposition. Smoking and coffee/tea consumption are associated with lower risk, while dairy intake increases risk. Anti-inflammatory drugs and physical activity reduce risk. Environmental exposures, such as pesticides, are linked to higher PD risk, with mechanisms involving mitochondrial dysfunction and inflammation. Prevention strategies include primary (population-wide), secondary (targeted at high-risk individuals), and tertiary (for established disease). Non-pharmacological interventions, such as physical activity, show promise. Population-based approaches, like promoting physical activity, could significantly reduce PD incidence. Challenges include ensuring accurate diagnosis and addressing disparities in healthcare access. Future research needs include better epidemiological data, harmonized prevention strategies, and understanding environmental and genetic interactions. Collaboration across disciplines is crucial for advancing PD prevention and treatment.The epidemiology of Parkinson's disease (PD) shows significant variations in time, geography, ethnicity, age, and sex. Prevalence has increased globally, partly due to reduced competing causes of death. Incidence is less certain, especially in low- and middle-income countries. PD is more common in older adults and men, with environmental factors like exposure to neurotoxins contributing to risk. Ethnic differences in disease risk exist, though they may reflect healthcare access disparities. PD is multifactorial, involving both genetic and environmental factors. Risk factors (e.g., pesticides) and protective factors (e.g., physical activity) are implicated, though causality is complex due to the long prodromal period. Public health strategies are needed for primary, secondary, and tertiary prevention. International collaboration is essential to enhance understanding and prevention of PD globally. PD diagnosis is based on clinical features, with biomarkers being explored for preclinical detection. Genetic factors, such as mutations in LRRK2, CHCHD2, VPS35, SNCA, PARKIN, DJ1, and PINK1, are associated with monogenic forms. The UK Brain Bank and MDS criteria are widely used for diagnosis. Diagnostic accuracy varies, and biomarker assays may help distinguish PD from other parkinsonian syndromes. Epidemiological studies show increasing prevalence, particularly in low- and middle-income countries, linked to longevity and environmental factors. Age is a key risk factor, with higher undiagnosed cases in older adults. Men have a higher incidence and mortality risk than women, though the exact reasons are unclear. Socioeconomic status is associated with disease risk, with lower status individuals facing greater exposure to neurotoxins. Determinants of PD include environmental toxins (pesticides, solvents, air pollution), lifestyle factors (diet, physical activity, smoking), and genetic predisposition. Smoking and coffee/tea consumption are associated with lower risk, while dairy intake increases risk. Anti-inflammatory drugs and physical activity reduce risk. Environmental exposures, such as pesticides, are linked to higher PD risk, with mechanisms involving mitochondrial dysfunction and inflammation. Prevention strategies include primary (population-wide), secondary (targeted at high-risk individuals), and tertiary (for established disease). Non-pharmacological interventions, such as physical activity, show promise. Population-based approaches, like promoting physical activity, could significantly reduce PD incidence. Challenges include ensuring accurate diagnosis and addressing disparities in healthcare access. Future research needs include better epidemiological data, harmonized prevention strategies, and understanding environmental and genetic interactions. Collaboration across disciplines is crucial for advancing PD prevention and treatment.