Alpha-synuclein (αSyn)-related pathology crucially contributes to the pathogenesis of Parkinson’s disease (PD), leading to progressive neuronal populations loss in specific brain regions. This results in the presence of both motor and non-motor symptoms in PD patients. Anxiety occurs at an early stage of the disease and is one of the most frequent neuropsychiatric symptoms in patients with PD, indicating pathology in the cortico-limbic system. This study aimed to decipher that the spread of αSyn pathology to a given brain region is sufficient to induce non-motor symptoms observed in PD patients, while psychiatric symptoms of fear and anxiety may originate from pathology in the basolateral amygdala (BLA).Bilateral stereotaxic injection of human αSyn-preformed amyloid fibrils (PFFs) in BLA or striatum (STR) was conducted in female mice overexpressing human αSyn (Thy1-αSyn) and wild-type (WT) littermates. We characterized the spread of αSyn pathology across brain regions and examined the behavioral and fear responses in mice at one-month post-injection (mpi) and 2 mpi of PFFs.Injection of PFFs resulted in increased pathological αSyn accumulation in Thy1-αSyn and WT mice, compared to control (phosphate-buffered saline). Thy1-αSyn mice exhibited increased cue-related fear behavior 1 mpi of PFFs into the BLA, while contextual fear was neither affected by treatment nor genotype. Notably, WT displayed enhanced contextual fear 2 mpi of PFFs into the STR compared to PBS control. These findings imply that αSyn-related pathology may disrupt the amygdala-striatal pathway, leading to enhanced fear responses in animal models of PD.