Fusobacterium periodonticum promotes colorectal tumorigenesis via decanoic acid-driven neutrophil chemotaxis.

Post-traumatic stress disorder (PTSD) is a debilitating psychiatric condition characterized by re-experiencing, avoidance, negative emotions and thoughts, and hyperarousal following exposure to severe trauma. A core cognitive mechanism underlying PTSD symptom severity is negative interpretation bias—the tendency to perceive ambiguous stimuli as threatening. This cognitive distortion leads individuals to perceive their environment as more dangerous than it is, contributing to persistent fear responses and difficulties in emotional regulation. Empirical evidence indicates that PTSD symptom severity is associated with negative interpretation bias, and modifying this bias may help alleviate PTSD symptoms. A growing body of evidence has linked negative interpretation bias to dysfunction within the amygdala—a key structure involved in fear regulation and expression, and a central hub for PTSD-related hypervigilance and heightened fear perception. Neuroimaging studies consistently demonstrate heightened amygdala responses to fear-related stimuli in individuals with PTSD, and exaggerated amygdala responses to neutral stimuli have also been observed and correlate with PTSD symptom severity. This over-responsivity suggests that the amygdala plays a critical role in assigning threat value to ambiguous stimuli, directly contributing to negative interpretation bias. However, these findings are primarily correlational, leaving the causal relationship between amygdala dysfunction and negative interpretation bias unresolved. Focal amygdala lesions provide a critical opportunity to establish a causal link between amygdala function and negative interpretation bias. Indeed, chronic focal disruption of amygdala activity alters fear perception and cognitive biases. Studies in non-PTSD individuals have shown that amygdala damage preferentially reduces sensitivity to fearful and other negative emotional expressions, while processing of positive emotions such as happiness remains largely intact. In a landmark study, Adolphs and colleagues demonstrated that patients with chronic bilateral amygdala lesions showed markedly lower recognition accuracy for fearful faces, while their perception of other emotions, including happiness, remained normal. This valence-specific blunting of responses to fear-related stimuli suggests a specific role of the amygdala in negative emotional processing. These observations raise the possibility that amygdala lesions could relieve negative interpretation bias and reduce PTSD symptoms by disrupting maladaptive fear evaluation processes. Notably, our prior work demonstrated that right amygdala and hippocampus ablation in the context of temporal lobe epilepsy was associated with PTSD symptom improvement; and at the neural level, pre- to post-ablation functional neuroimaging during a task contrasting fearful and neutral faces revealed reduced hyperactivation of the intact left amygdala and bilateral dorsal anterior cingulate cortex—neural changes paralleling those observed with PTSD symptom amelioration. However, it remained unclear whether these benefits stemmed from direct amygdala disruption solely or from secondary effects of contemporaneous hippocampal ablation and seizure reduction.