BackgroundPost-stroke depression (PSD) is one of the most frequent psychiatric disorders after stroke. However, the underlying brain mechanism of PSD remains unclarified. Using the amplitude of low-frequency fluctuation (ALFF) approach, we aimed to investigate the abnormalities of neural activity in PSD patients, and further explored the frequency and time properties of ALFF changes in PSD. MethodsResting-state fMRI data and clinical data were collected from 39 PSD patients (PSD), 82 S patients without depression (Stroke), and 74 age- and sex-matched healthy controls (HC). ALFF across three frequency bands (ALFF-Classic: 0.01–0.08 Hz; ALFF-Slow4: 0.027–0.073 Hz; ALFF-Slow5: 0.01–0.027 Hz) and dynamic ALFF (dALFF) were computed and compared among three groups. Ridge regression analyses and spearman’s correlation analyses were further applied to explore the relationship between PSD-specific alterations and depression severity in PSD. ResultsWe found that PSD-specific alterations of ALFF were frequency-dependent and time-variant. Specially, compared to both Stroke and HC groups, PSD exhibited increased ALFF in the contralesional dorsolateral prefrontal cortex (DLPFC) and insula in all three frequency bands. Increased ALFF in ipsilesional DLPFC were observed in both slow-4 and classic frequency bands which were positively correlated with depression scales in PSD, while increased ALFF in the bilateral hippocampus and contralesional rolandic operculum were only found in slow-5 frequency band. These PSD-specific alterations in different frequency bands could predict depression severity. Moreover, decreased dALFF in contralesional superior temporal gyrus were observed in PSD group. LimitationsLongitudinal studies are required to explore the alterations of ALFF in PSD as the disease progress. ConclusionsThe frequency-dependent and time-variant properties of ALFF could reflect the PSD-specific alterations in complementary ways, which may assist to elucidate underlying neural mechanisms and be helpful for early diagnosis and interventions for the disease.