Abstract: Ischemic stroke has a higher survival rate and is more likely to result in cognitive impairment than hemorrhagic stroke. The primary pathological mechanism underlying cognitive impairment involves dysfunction of neural circuits and damage to specific brain regions. This review aims to investigate the role of the hippocampus in cognitive impairment following a stroke. A review of the literature suggests that the hippocampus is a metabolically active structure that is easily involved in various metabolic states, such as hypoxia and hypoglycaemia. The functional changes in hippocampal cells associated with poststroke cognitive impairment mainly manifest as neuronal apoptosis, impaired synaptic plasticity, and decreased neurogenesis. The primary pathological mechanism of poststroke cognitive impairment involves a complex cascade of reactions, including neuroinflammatory activation, bursts of oxidative stress, and neuronal apoptosis induced by mitochondrial dysfunction. Interventional drugs for cognitive impairment after cerebral ischemia include neuroprotective drugs, traditional Chinese medicines and their extracts, and stem cell therapies. Many of these drugs have unique advantages, including the inhibition of neuroinflammation, the prevention of apoptosis, and the promotion of neurogenesis. They hold great potential for the prevention and treatment of cognitive impairment following cerebral ischemia. However, most current studies are animal experiments, and relatively few clinical studies exist. In future research, emphasis should be placed on interventions for cognitive impairment following cerebral ischemia. These findings offer novel perspectives for the treatment of cognitive impairment after cerebral ischemia. Finally, the role of hippocampal cell dysfunction in other diseases associated with cognitive decline is briefly discussed. The aim of this review is to provide researchers with a comprehensive overview of the role of the hippocampus in cognitive impairment and its intervention strategies. 

Key words: apoptosis, cerebral ischemia model, cognitive decline, hippocampal neurons, hippocampus, mitochondrial dysfunction, neuroinflammation, neuroprotection, neurovascular unit, poststroke cognitive impairment