Mitochondrial health and redox imbalance in the context of learning and memory in post-subarachnoid haemorrhage: therapeutic strategies for recovery

Abstract

Subarachnoid hemorrhage constitutes 5-10% of all strokes and is a subtype of hemorrhagic stroke that imposes a significant financial burden on medical care because it often affects younger people and has a high mortality rate with few treatment choices and poor patient outcomes. Preventing rebleeding, treating SAH patients as soon as possible, and preventing delayed cerebral ischemia (DCI) are important objectives during early brain injury (EBI) or first 72 hrs. Cerebral vasospasm and DCI continue to be issues despite surgical advances, particularly in older patients. A delayed diagnosis can result in DCI, which is linked to redox imbalance or oxidative stress (O.S) that causes learning-memory deficit, inflammation, apoptosis, mitophagy, disruption to the blood-brain barrier, and other detrimental processes that exacerbate these disorders. Individuals over 50 are susceptible to SAH, and as we age, our body's excessive oxidative stress increases our risk of hemorrhagic stroke. This review highlights innovative approaches that target mitochondria for the treatment of SAH and emphasizes their role in learning, memory, EBI and DCI post-SAH, as well as their therapeutic potential.

Keywords: Apoptosis; Delayed cerebral ischemia; Early brain injury; Learning and memory; Oxidative stress; Subarachnoid hemorrhage.