Abstract
Post-stroke dementia is a consequence of neuronal cell death and ongoing cellular injury following stroke. The initial phase after stroke involves early neuronal injury due to ischemia or hemorrhage, followed by injury occurring during the reperfusion process. Current primary treatment methods—such as recanalization with thrombolytic agents or mechanical thrombectomy—help protect against direct neuronal cell death and contribute substantially to functional recovery after stroke. Nevertheless, neuroprotection during the subsequent stages remains critically important and valuable for the prevention and treatment of post-stroke dementia. Therapeutic strategies applied during this phase focus on preventing acute-phase cellular injury, preventing reperfusion-phase injury, and promoting neuronal recovery. Numerous neuroprotective agents, such as cerebrolysin, have been studied and shown to be effective both in experimental research and in clinical practice, in their role of neuroprotection and neurotrophic support for neurological functional recovery.
