LAUSR

Mitochondria are cell organelles that initially had an independent existence as α-proteobacteria. A symbiotic arrangement with either a proto-eukaryote or an archaeon enabled the newly formed organism to generate levels of cellular energy that could sustain metabolic processes of previously impossible complexity (Gray, 2012). In this singular incident, the course of evolution was profoundly changed. Without mitochondria, multicellular organism might not be possible, and there is no doubt that human life depends on them. Chief among the many different tasks of mitochondria is ATP production in the respiratory chain. While the brain contributes less than 2% of the mass of a human body, it consumes 20% of all energy expensed. Despite this vast demand for ATP, the brain limits themetabolic pathways by which ATP is generated. Neurons, in particular, depend on mitochondrial respiration to generate the high amounts of ATP needed to maintain basic cellular homeostasis, precise electrical activity, and synaptic function. Small aberrations inmitochondrial respiratory capacity can cause neuronal malfunction and contribute to neuropsychiatric disorders, while having minimal physical impact or cellular consequences outside the brain, where alternative pathways to ATP synthesis are more readily available. Neuropsychiatric disorder research has been constrained by an emphasis on structure-function relationships, and by the search for disease-causing factors that are specific to the brain. However, biological processes are not just defined by structural parameters, but also by energy states (Picard et al., 2016). Unlike inanimate objects, life itself is defined by energy. Additionally, it is becoming increasingly accepted