Apathy is a common neuropsychiatric disease after stroke and is linked to a lower quality of life while undergoing rehabilitation. However, it is still unknown what are the underlying neural mechanisms of apathy. This research aimed to explore differences in the cerebral activity and functional connectivity (FC) of subjects with post-stroke apathy and those without it. A total of 59 individuals with acute ischemic stroke and 29 healthy subjects with similar age, sex, and education were recruited. The Apathy Evaluation Scale (AES) was used to evaluate apathy at 3 months after stroke. Patients were split into two groups—PSA (n= 21) and nPSA (n= 38)—based on their diagnosis. The fractional amplitude of low-frequency fluctuation (fALFF) was used to measure cerebral activity, as well as region-of-interest to region-of-interest analysis to examine functional connectivity among apathy-related regions. Pearson correlation analysis between fALFF values and apathy severity was performed in this research. The values of fALFF in the left middle temporal regions, right anterior and middle cingulate regions, middle frontal region, and cuneus region differed significantly among groups. Pearson correlation analysis showed that the fALFF values in the left middle temporal region (p< 0.001, r = 0.66) and right cuneus (p< 0.001, r = 0.48) were positively correlated with AES scores in stroke patients, while fALFF values in the right anterior cingulate (p< 0.001, r = −0.61), right middle frontal gyrus (p< 0.001, r = −0.49), and middle cingulate gyrus (p= 0.04, r = −0.27) were negatively correlated with AES scores in stroke patients. These regions formed an apathy-related subnetwork, and functional connectivity analysis unveiled that altered connectivity was linked to PSA (p< 0.05). This research found that abnormalities in brain activity and FC in the left middle temporal region, right middle frontal region, right cuneate region, and right anterior and middle cingulate regions in stroke patients were associated with PSA, revealing a possible neural mechanism and providing new clues for the diagnosis and treatment of PSA.