Neuroinflammation and Post-Stroke Depression: Focus on the Microglia and Astrocytes Post-stroke depression (PSD) is a common and disabling complication of stroke, affecting approximately one-third of stroke survivors. The exact pathogenesis of PSD is not fully understood, but neuroinflammation following stroke is considered a key underlying mechanism. During ischemic stroke, both astrocytes and microglia undergo morphological and functional changes, playing pro-inflammatory or anti-inflammatory roles in the pathological process. These cells exhibit dual roles in PSD due to phenotypic transformation. This review summarizes the latest evidence on neuroinflammation in PSD, focusing on the phenotypic transformation of microglia and astrocytes after ischemic stroke and revealing their dual roles in PSD through modulating neuroinflammation. PSD is associated with sleep disorders, disability, cognitive impairment, poor rehabilitation outcomes, social withdrawal, and increased mortality. It has been a focus of research since the 1905 treatise "Depressive States in Old age." The link between depression and atherosclerotic disease was first established in 1955. Depression is more common in stroke patients, attracting significant research attention. PSD is diagnosed using DSM-5 criteria, requiring at least five symptoms lasting at least two weeks. The Hamilton Depression Rating Scale (HDRS) and Patient Health Questionnaire-9 (PHQ-9) are used for screening. PSD occurs at any time after stroke, with 31.72% of patients showing depression within two weeks of stroke onset. The frequency of PSD varies based on diagnostic methods, time of assessment, and study populations. The frequency of PSD is related to lesion location. Lesions in the left hemisphere, particularly the frontal region, are associated with higher depression risk. Stroke in the left hemisphere cortex is linked to early onset of PSD. Stroke patients with left posterior lesions have higher depression frequency than those with right anterior lesions. Stroke patients with left subcortical or cortical anterior lesions have more severe depression. Neuroinflammation is a dominant factor in depressive disorders. Inflammatory mediators such as cytokines and reactive oxygen species are closely related to PSD development. Pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α are released after ischemic stroke, exacerbating neuroinflammation and brain injury. Anti-inflammatory cytokines like IL-10 have protective effects against depression. Microglia, the resident immune cells in the CNS, undergo phenotypic transformation after stroke, with M1 microglia being pro-inflammatory and M2 microglia being anti-inflammatory. M1 microglia polarization promotes neuroinflammation and immune reactions after stroke. M2 microglia have neuroprotective effects. Astrocytes also play dual roles in PSD. A1 astrocytes produce pro-inflammatory cytokines, exacerbating neuroinflammationNeuroinflammation and Post-Stroke Depression: Focus on the Microglia and Astrocytes Post-stroke depression (PSD) is a common and disabling complication of stroke, affecting approximately one-third of stroke survivors. The exact pathogenesis of PSD is not fully understood, but neuroinflammation following stroke is considered a key underlying mechanism. During ischemic stroke, both astrocytes and microglia undergo morphological and functional changes, playing pro-inflammatory or anti-inflammatory roles in the pathological process. These cells exhibit dual roles in PSD due to phenotypic transformation. This review summarizes the latest evidence on neuroinflammation in PSD, focusing on the phenotypic transformation of microglia and astrocytes after ischemic stroke and revealing their dual roles in PSD through modulating neuroinflammation. PSD is associated with sleep disorders, disability, cognitive impairment, poor rehabilitation outcomes, social withdrawal, and increased mortality. It has been a focus of research since the 1905 treatise "Depressive States in Old age." The link between depression and atherosclerotic disease was first established in 1955. Depression is more common in stroke patients, attracting significant research attention. PSD is diagnosed using DSM-5 criteria, requiring at least five symptoms lasting at least two weeks. The Hamilton Depression Rating Scale (HDRS) and Patient Health Questionnaire-9 (PHQ-9) are used for screening. PSD occurs at any time after stroke, with 31.72% of patients showing depression within two weeks of stroke onset. The frequency of PSD varies based on diagnostic methods, time of assessment, and study populations. The frequency of PSD is related to lesion location. Lesions in the left hemisphere, particularly the frontal region, are associated with higher depression risk. Stroke in the left hemisphere cortex is linked to early onset of PSD. Stroke patients with left posterior lesions have higher depression frequency than those with right anterior lesions. Stroke patients with left subcortical or cortical anterior lesions have more severe depression. Neuroinflammation is a dominant factor in depressive disorders. Inflammatory mediators such as cytokines and reactive oxygen species are closely related to PSD development. Pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α are released after ischemic stroke, exacerbating neuroinflammation and brain injury. Anti-inflammatory cytokines like IL-10 have protective effects against depression. Microglia, the resident immune cells in the CNS, undergo phenotypic transformation after stroke, with M1 microglia being pro-inflammatory and M2 microglia being anti-inflammatory. M1 microglia polarization promotes neuroinflammation and immune reactions after stroke. M2 microglia have neuroprotective effects. Astrocytes also play dual roles in PSD. A1 astrocytes produce pro-inflammatory cytokines, exacerbating neuroinflammation