CSF alpha-Synuclein Seed Amplification Assay results in routine clinically collected samples.

Mental health disorders are a leading cause of disability globally, with prevalence estimates continuing to rise (Network, ; World Health Organization, ). Childhood adversity remains one of the strongest predictors of later psychopathology, with lifetime risk doubling for those who experience childhood adversity (Green et al., ; Kisely et al., ; Li, d'Arcy, & Meng, ; McLaughlin et al., ). In a global study spanning 21 countries, approximately 38% of individuals reported experiencing at least one form of adversity during childhood, with more recent estimates suggesting rates as high as 60% (Kessler et al., ; Madigan et al., ). The eradication of childhood adversity was estimated to reduce the prevalence of mental health disorders by up to 42% globally (Kessler et al., ). However, optimal targets and timing for intervention remain unclear, particularly for children in low‐ and middle‐income countries (LMIC). Gaining a clearer understanding of how the type and timing of childhood adversity impacts risk for mental health disorders is an important step towards developing effective and cost‐efficient prevention and intervention efforts (Schaefer, Cheng, & Dunn, ). Historically, childhood adversity research has disproportionally focused on WEIRD (Western, Educated, Industrialized, Rich, and Democratic) samples, despite 88% of the world's children residing in low‐ and middle‐income settings (Ceccarelli et al., ; Henrich, Heine, & Norenzayan, ; Network, ). Understanding the relationships between childhood adversities and risk for mental health disorders in LMIC is crucial to expanding the generalizability of results and informing the adaptation of interventions to differing cultural and socioeconomic contexts. Children in LMIC countries, such as South Africa, are exposed to higher rates of adversity including intimate partner violence, parental substance abuse, and traumatic events (Ceccarelli et al., ; Stein et al., ). One study comparing longitudinal birth cohorts found 91% of participants from a South African cohort experienced at least one childhood adversity by age 10 years, compared with 64% and 67% in British and Dutch cohorts, respectively (Bigler et al., ). Further, studies examining adversities generally focus on individual‐level adversities, such as interpersonal trauma, rather than community‐ and systemic‐level factors, such as exposure to community violence and chronic food insecurity (Stirling, Toumbourou, & Rowland, ). Children in LMIC are disproportionately exposed to these macro‐level adversities, and increasing evidence points to their negative impact on psychopathology risk (Hyde, Gard, Tomlinson, Suarez, & Westerman, ). Additionally, given that parental stress is biologically and psychologically correlated with child stress and has been linked to child emotional and behavioral problems (Melinder et al., ; Najman et al., ; Ribas, Montezano, Nieves, Kampmann, & Jansen, ), it is crucial to consider not only direct exposures to the child, but also indirect exposures via parental experiences such as maternal adverse events. Beyond examining the of childhood adversity that influence risk for psychopathology, it is also vital to understand how of exposure may alter risk. Evidence from a recent systematic review (Schaefer et al., ) and empirical studies suggest both type and timing of childhood adversity influence the development of childhood psychopathology (i.e., internalizing and externalizing) symptoms, which are early indicators of later psychopathology risk (Dunn et al., ; Farooq et al., ; Juen et al., ). Life‐course theory proposes the timing of adversity exposure may differentially impact outcomes, based on: exposure during a of development, of exposure across childhood, and the of an exposure. Sensitive period hypotheses posit there are specific developmental periods when an exposure disproportionately impacts outcomes (Ben‐Shlomo & Kuh, ; Frankenhuis & Fraley, ; Schaefer et al., ). Accumulation hypotheses contend that the number of exposures linearly increases risk, regardless of timing (Evans, Li, & Whipple, ; Guidi, Lucente, Sonino, & Fava, ; Slopen, Meyer, & Williams, ). Recency hypotheses argue adversities occurring closer to the timing of the outcome have stronger effects (Shanahan, Copeland, Costello, & Angold, ). Research conducted in HIC contexts, like the United Kingdom and the Netherlands, provides mixed evidence for developmental timing (Bagner, Pettit, Lewinsohn, & Seeley, ; Yoon, ), accumulation (Buss, Davis, & Kiel, ; Hogye, Lucassen, Jansen, Schuurmans, & Keizer, ; Mäntymaa et al., ; Rogosch, Dackis, & Cicchetti, ), and recency of exposure (Dunn et al., ) predicting childhood psychopathology symptoms. Very few studies have examined which life‐course hypotheses best explain child psychopathology symptoms in LMIC contexts, with a single cross‐sectional study conducted in Tanzania finding the recency of exposure as the strongest predictor of childhood psychopathology compared t