This body of research investigated the influence of neuroendocrine and genetic elements of arousal on cognitive processes in the development of intrusive memories and flash-forward intrusions as related to Post-Traumatic Stress Disorder. Specifically, this thesis investigated various mechanisms that may underlie intrusive symptoms as postulated by prevalent theories of PTSD. Study 1 examined the distinctive relationship between peritraumatic dissociation and subsequent re-experiencing symptoms. Network analyses revealed strong positive edges between peritraumatic dissociation and subsequent amnesia, as well as the re-experiencing symptoms of physical reactivity to reminders, flashbacks, intrusions, and dreams, and to a lesser extent emotional numbness and hypervigilance. The finding that peritraumatic dissociation is related to subsequent re-experiencing symptoms is consistent with cognitive models that emphasize the role of dissociative experiences during a traumatic event in the etiology of PTSD re-experiencing symptoms. Study 2 aimed to determine whether peri-traumatic stress, as measured via salivary cortisol and salivary alpha-amylase, as well as pre-existing genetic polymorphisms on the FKBP5 gene increased dissociation and data-driven processing, and subsequently impacted intrusive memories related to a trauma film. The findings revealed that greater noradrenergic arousal predicted less intrusive memory distress in individuals who scored higher on data-driven processing and trait dissociation, and in FKBP5 low-risk carriers. For individuals who reported less data-driven processing and trait dissociation, and in FKBP5 high-risk carriers, as noradrenergic arousal increased, intrusive memory distress increased. This study also showed no association between data-driven processing with memory fragmentation, and fragmentation with intrusive memories. Whilst these findings support some aspect of cognitive models of PTSD as they indicate a role for data-driven processing and dissociation in intrusive symptoms, they highlight a threshold at which these variables stop moderating the relationship between arousal and intrusive memories and suggest that memory fragmentation is not related to intrusive memories. Study 3 examined the role of cognitive control in flash-forward intrusions in the context of an enduring stressor, the COVID-19 pandemic. In line with expectations, results showed that as cognitive control worsened, FKBP5 high-risk carriers reported more flash-forward distress, and low-risk carriers reported less distress. These findings are considered in the context of hippocampal changes and are consistent with emerging theories of PTSD. Lastly, study 4 sought to investigate the role of two neurological processes, pattern separation and pattern completion in intrusive memories in individuals with PTSD compared to trauma exposed controls. Consistent with existing literature, the data indicate that individuals with PTSD reported more data-driven processing, more intrusive symptoms, and demonstrated better behavioural pattern completion than trauma-exposed controls. These findings are in line with current cognitive models of PTSD, as they again indicate a role for data-driven processing in PTSD. However, study 4 found no support for the postulate that deficient pattern separation is a feature of PTSD and found an opposite effect for the role of pattern completion. Whilst these findings are inconsistent with theory, they are in line with existing experimental studies. Overall, the findings from this thesis provide insight into cognitive and biological models of PTSD and shed light on the mechanisms underlying the nature and development of intrusive symptoms