Childhood adversity has been implicated in poorer developmental outcomes such as behavioral problems, poorer mental health and cognitive deficits. Studies have also linked adversity to alterations in cortical brain structures. To date however, almost all knowledge of the effects of adversity on outcomes has come from cross-sectional studies or longitudinal studies that used cross-sectional data analysis method. In an attempt to bridge this gap, across three empirical studies, this thesis sets out to implement series of longitudinal data modelling aimed at disentangling the intricacies of the effects of childhood adversity on mental health, cognitive abilities and brain development. In study 1, I analyzed a large sample (N=13,287) of 5 wave longitudinal data obtained from the Millennium Cohort Study in an attempt to understand how early-life adversity, mental health and cognition affect one another or how the effects unfold over time. To achieve this, I used focused longitudinal mediation model via path model approach. Results showed that early-life adversity was associated with poorer performance in spatial working memory and vocabulary performance. Notably, current and previous mental health mediated a substantial proportion (working memory: 59%; vocabulary: ¬70%), of these effects. Findings also showed that adversity has an enduring adverse effect on mental health, and that poorer mental health is associated with poorer cognitive performance later on in development. Moreover, the adverse effects of mental health were cumulative: poor mental health early on is associated with poorer cognitive scores up to 11 years later, above and beyond contemporaneous mental health. Based on this evidence, I suggested that the academic and cognitive competence of vulnerable children may be enhanced if their early mental health conditions are given deliberate clinical attention. In a follow-up study 2, I attempted to provide empirical support for dimensional model of adversity which argues that childhood adversity can be classified into subgroups, known as dimensions. For this purpose, I analyzed rich set of adverse childhood experiences obtained from a subset of ALSPAC cohort sample (N = 2,965) using latent class analysis. Findings showed evidence of five distinct adversity subgroups, namely, low adversity, dysfunctional family, parental deprivation, family poverty and global adversity. To establish a pathway to cognitive functioning among the adversity subgroups, a further analysis using latent class regression revealed that family poverty subgroup performed poorest in working memory and inhibition tasks. A separate analysis revealed that the effects of each individual adversity types on cognitive outcomes were mostly consistent with the observed class performance in which they co-occurred. Regardless, sensitive periods (timing of adversity exposure) explained more variability in these observed effects compared to accumulation hypothesis. In study 3, I analysed a subset of IMAGEN cohort sample (N = 502) using latent change score model and complete longitudinal mediation model via autoregressive path approach, aimed to understand the long-term interrelations between adverse life events, cortical development and cognitive functioning. Results of latent change score model showed that greater baseline adverse life events predicted a marginal reduction in the right anterior cingulate surface area. In addition, baseline right orbitofrontal cortical thickness predicted a decrease change in adverse life events. I found no evidence of association between adverse life events and volumes of cortical structures or cognitive outcomes. In separate longitudinal analyses, I found no evidence of indirect effects in the two neurocognitive pathways that link adverse life events in adolescence to brain and cognitive outcomes. Although the results of latent change score model appear to support the robust cross-sectional studies which have implicated adverse events in brain alterations, especially in the prefrontal, however, the magnitude of effects observed in this study 3 are smaller than have been reported in the cross-sectional studies, suggesting that potential long-term impact of adverse life events on brain structures may likely be more modest than previously noted. I end the thesis by articulating the implications of these findings across the 3 empirical studies, indicating the strengths and limitations, and suggesting areas for future directions. Generally, it is my hope that new insight drawn from these longitudinal studies will inform the right policies in the society. Such policies may include but not limited to increase clinical intervention for the vulnerable and most underprivileged children as well greater financial aids to families living in poverty, given recent reports that such aid package can alter the trajectories of developmental outcomes of children in a positive way.