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Background/Objectives: Wildfires are increasing in frequency and intensity worldwide, leading to widespread exposure to wildfire smoke and associated environmental stressors. While the respiratory and cardiovascular effects of wildfire smoke are well established, the potential neurological and mental health consequences have received growing attention. This narrative review synthesizes evidence from animal and human studies examining the effects of wildfire exposure on neurological function, behavior, and mental health, and explores the potential role of epigenetic mechanisms. Methods: A structured literature search was conducted using PubMed to identify original research articles examining wildfire exposure in relation to neurological, behavioral, mental health, or epigenetic outcomes. Both human and animal studies were included. Results: Experimental animal studies suggest that wildfire smoke exposure can induce neuroinflammation, blood-brain barrier disruption, metabolic alterations, and behavioral changes. Human studies conducted in wildfire-affected populations frequently report an elevated prevalence of depression, anxiety, post-traumatic stress disorder (PTSD), and sleep disturbances. However, many of these studies reflect mental health outcomes associated with wildfire disaster exposure, including evacuation and psychosocial stress, whereas only a subset of studies quantify wildfire smoke or PM_2.5 exposure. Emerging evidence from both animal models and human studies indicates that wildfire exposure may be associated with changes in epigenetic regulation, including alterations in DNA methylation and miRNA expression. Conclusions: Current evidence suggests that wildfire exposure may influence neurological and mental health outcomes through biological and psychosocial pathways. However, the literature remains heterogeneous, and the independent effects of wildfire smoke exposure are often difficult to disentangle from disaster-related stressors. In addition, human evidence linking wildfire exposure to epigenetic changes remains limited, restricting causal inference. Further longitudinal and mechanistic studies integrating exposure assessment, neurological outcomes, and molecular profiling are needed to clarify these relationships.