Lifestyle Factors, Mitochondrial Dynamics, and Neuroprotection

Abstract

The brain requires vast amounts of energy to carry out neurotransmission; indeed, it is responsible for approximately one-fifth of the body’s energy consumption. Therefore, in order to understand functions of brain cells under both normal and pathological conditions, it is critical to elucidate dynamics of intracellular energy. The mitochondrion is the key intercellular organelle that controls neuronal energy and survival. Numerous studies have reported a correlation between altered mitochondrial function and brain-associated diseases; thus mitochondria may serve as a promising target for treating these conditions. In this chapter, we will discuss the mechanisms of mitochondrial production, movement, and degradation in order to understand accessibility of energy during physiological and pathological conditions of the brain. While research targeting molecular dynamics is promising, translation into clinical relevance based on bench research is challenging. For these reasons, we will also summarize lifestyle factors, including interventions and chronic comorbidities that disrupt mitochondrial dynamics. By determining lifestyle factors that are readily accessible, we can propose a new viewpoint for a synergistic and translational approach for neuroprotection.

The effects of acute Methylene Blue administration on cerebral blood flow and metabolism in humans and rats

“…This unmet need led to a recent growth of interest in identification of neuroprotective strategies aiming to revert the dysfunction of neuronal mitochondrial respiration. [7][8][9][10] To this end, one plausible strategy is to enhance cerebral oxygen consumption via boosting the mitochondrial oxidative phosphorylation and adenosine triphosphate (ATP) production.…”

The effects of acute Methylene Blue administration on cerebral blood flow and metabolism in humans and rats

“…Compounds used as routine clinical treatments for these conditions do not address the associated neuro-energetic deficits or reverse the observed metabolic decline. This unmet need led to a recent growth of interest in identification of neuroprotective strategies aiming to revert the dysfunction of neuronal mitochondrial respiration [7][8][9][10] . To this end, one plausible strategy is to enhance cerebral oxygen consumption via boosting the mitochondrial oxidative phosphorylation and adenosine triphosphate (ATP) production.…”