This proposal leverages the infrastructure and science of the parent study R01 ES030039 that currently aims to identify early adult brain and behavioral risk indicators for parkinsonism in a minority cohort followed since birth as part of the Columbia Center for Children’s Environmental Health. We now propose to apply our risk assessment methods to better understand the pathogenesis of Alzheimer’s Disease (AD) in this same cohort of African American and Dominican American young adults—race/ethnic populations with the highest rates of AD, yet underrepresented in research studies. AD is the most common progressive neurodegenerative disorder, now understood to be a chronic ‘age-related’ disease beginning with an asymptomatic preclinical phase, progressing to a symptomatic pre-dementia phase (mild cognitive impairment or MCI), and concluding with memory loss, functional decline and dementia. AD is characterized by abnormal build-up of proteins that form amyloid plaques and tau tangles in the brain, a process that may underlie cognitive decline. Currently, there is a lack of high quality biologic data on risk indicators, preclinical brain and behavioral changes, and very early disease progression in minority populations, posing critical barriers to understanding how disease processes operate in different race/ethnic groups. The parent study includes measures of extrapyramidal function, sleep behavior, autonomic function, olfactory deficits, executive function, cognitive function or impairment, gait, tremor and structural magnetic resonance imaging obtained at 18-21 years of age—all of which may provide vital information on baseline risk for AD in this sample. This cohort is unique in having a previously-collected biomarker of exposure to chlorpyrifos (CPF), a broad-spectrum organophosphate insecticide known to be an environmental risk factor for both Parkinson’s (PD) and AD, permitting us to classify our sample by level of potential environmental risk for neurodegenerative disease. In this supplement, using parent study data, we will first characterize the current cognitive, neurological, and behavioral ‘health’ of the cohort in early adulthood using previously-collected data, to derive a multi-modal profile of baseline capital reserve. To these data, we will add several new cognitive measures to tap memory and visuoperceptual functions at 22 years. Second, applying an algorithm developed by Provenzano (co-investigator on this supplement) to T1w neuroimaging data collected in the parent study, we will estimate the divergence between chronological age and estimated brain age. Third, we will test associations between this divergence (from Aim 2) and the profile of cognitive, neurological, and behavioral ‘health’ (from Aim 1). To this model, we will add the biomarker of CPF exposure to assess the contribution of a toxic exposure to the baseline profile and brain age divergence. Establishing these baseline data for brain and behavioral health in early adu...