Objective: Parkinson's disease (PD) is a progressive neurodegenerative disease, which is characterized by severe motor symptoms such as bradykinesia, tremor, and rigidity. Degeneration is characterized by progressive loss of dopaminergic neurons in the substantia nigra. Mild Cognitive Impairment (PD-MCI), emerges as one of the major risk factors for PD Dementia (PDD). Revealing the markers associated with cognitive impairment with neuroimaging may play a critical role in the early diagnosis of the disease and early treatment. Methods: 28 PD Patients with Mild Cognitive Impairment (PD-MCI) and 27 cognitively normal PD patients (PD-CN) who were statistically similar in terms of mean education years, age, and gender were included. Functional magnetic resonance imaging (fMRI) data were collected with a 3T MRI (Phillips, Achieva, The Netherlands). Fractional amplitudes of low-frequency fluctuations (fALFF) of resting-state blood-oxygenlevel-dependent (BOLD) signal were calculated at the voxel level. after preprocessing steps with CONN (https://web.conntoolbox. org/) software. Clusters with significant differences in fALFF values between the groups were calculated using the general linear model with a statistical threshold of puncorr< 0.001 at the voxel level and pFDR <0.05 corrected at the cluster level. Clusters with 100 or more voxels were evaluated. Results: In the PD-MCI group, fALFF values were found to be significantly lower in the temporal pole and insular cortex in the left hemisphere and in the insular cortex in the right hemisphere, when compared to the PD-CN group. Conclusion: In the PD-MCI group, compared to the PD-CN group, reduction of the D2 receptor availability in the bilateral insula was previously demonstrated by Positron Emission Tomography (PET). This finding in PET, which requires the use of radioactive agents, has not yet been demonstrated in fMRI. In this study, fALFF decreases, observed in bilateral insula, highlight the importance of insular circuits in cognitive impairment in PD, and also sheds light on the neurochemical mechanisms of BOLD signal. [ABSTRACT FROM AUTHOR]