Neuroprotective methodologies of Co-enzyme Q10 associated mitochondrial dysfunction in post brain hemorrhagic treatment: Clinical and pre-clinical findings.

Cerebral brain hemorrhage is associated with the highest mortality and morbidity despite only constituting approximately 10-15% of all strokes classified into intracerebral and intraventricular hemorrhage where most of the patients suffer from impairment in memory, weakness or paralysis in arms or legs, headache, fatigue, gait abnormality and cognitive dysfunctions. Understanding molecular pathology and finding the worsening cause of hemorrhage will lead to explore the therapeutic interventions that could prevent and cure the disease. Mitochondrial ETC-complexes dysfunction has been found to increase neuroinflammatory cytokines, oxidative free radicals, excitotoxicity, neurotransmitter and energy imbalance that are the key neuropathological hallmarks of cerebral hemorrhage. Co-enzyme Q10 (CoQ10), as a part of the mitochondrial respiratory chain can effectively restore these neuronal dysfunctions by preventing the opening of mitochondrial membrane transition pore, thereby counteracting cell death events as well as exerts an anti-inflammatory effect by influencing the expression of NF-kB1 dependent genes thus preventing the neuroinflammation and energy restoration. Due to behavior and biochemical heterogeneity in post cerebral brain hemorrhagic pattern different pre-clinical autologous blood injection models are required to precisely investigate the forthcoming therapeutic strategies. Despite emerging pre-clinical research and resultant large clinical trials for promising symptomatic treatments, there are very less pharmacological interventions demonstrated to improve post operative condition of patients where intensive care is required. Therefore, in current review, we explore the disease pattern, clinical and pre-clinical interventions under investigation and neuroprotective methodologies of CoQ10 precursors to ameliorate post brain hemorrhagic conditions.