Abstract
The development of acute cerebral ischemia triggers pathobiochemical cascade reactions, the outcome of which is cerebral infarction (MI), which is formed by two mechanisms: necrotic cell death and apoptosis - programmed cell death. These modern pathogenetic concepts have made it possible to propose a sequence of stages »Based on their causal relationships. Each stage of the cascade is a target for the therapeutic effect of drugs, primarily with neuroprotective effects.
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