Evidence suggests that lifelong cumulative exposure to pesticides may generate lasting toxic effects on the central nervous system and contribute to the development of Alzheimer's disease (AD). A number of reports indicate a potential association between long-term/low-dose pesticide exposure and AD, but the results are inconsistent. Therefore, we conducted a meta-analysis to clarify this association. Relevant studies were identified according to inclusion criteria. Summary odds ratios (ORs) were calculated using fixed-effects models. A total of seven studies were included in our meta-analysis. A positive association was observed between pesticide exposure and AD (OR = 1.34; 95% confidence interval [CI] = 1.08, 1.67; n = 7). The summary ORs with 95% CIs from the crude and adjusted effect size studies were 1.14 (95% CI = 0.94, 1.38; n = 7) and 1.37 (95% CI = 1.09, 1.71; n = 5), respectively. The sensitivity analyses of the present meta-analysis did not substantially modify the association between pesticide exposure and AD. Subgroup analyses revealed that high-quality studies tended to show significant relationships. The present meta-analysis suggested a positive association between pesticide exposure and AD, confirming the hypothesis that pesticide exposure is a risk factor for AD. Further highquality cohort and case-control studies are required to validate a causal relationship.Alzheimer's disease (AD) is the most common progressive neurological disease and results in an irreversible loss of neurons 1 . Late-onset AD, which typically develops after age 60, is the most common form and is characterized by the insidious onset of dementia, progressive memory loss, and cognitive decline ultimately leading to dysfunction in daily life and work abilities 2 . Pathologically, amyloid plaques and neurofibrillary tangles are the main forms of aggregated proteins involved in AD. Amyloid plaques are visible protein aggregates derived from the dimers and oligomers of brain amyloid-β protein, while neurofibrillary tangles are composed of a compact filamentous network of helical filaments of hyperphosphorylated tau protein. Together these neuropathological changes are thought to result in the loss of synapses and neuronal cell death, leading in cognitive dysfunction 3,4 . The aetiology of late-onset AD remains largely unknown but is believed to be multifaceted, resulting from both genetic and environmental factors 5 . The main risk factor is clearly age, though research has identified some genetic risk factors that may account for a small percentage of AD cases 6 . The most well established genetic component of AD risk is the APOE-ε 4 allele 7,8 . Epidemiological studies have reported a higher prevalence of AD in rural areas than in urban settings. Over the past decades, pesticides have been used to increase the productivity and the specialization of cultures in rural areas 9 . Evidence from in-vitro models and animal studies suggests that long-term/low-dose pesticide exposure may lead to the neuronal loss in specific brain regi...