:
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. Coenzyme
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 preclinical
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.