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Researchers utilized an intention-to-treat analysis, which looks at the treatment participants were originally assigned whether or not participants received or properly followed the treatment protocol

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Moreover, mitochondrial dysfunction and related oxidative stress can activate the innate branch of the immune system, leading to the release of pro-inflammatory cytokines influencing various depression-related pathophysiological mechanisms: monoaminergic neurotransmission disruption, tryptophan degradation toward neurotoxic catabolites, glutamate-related excitotoxicity, decreased neurotrophic factors and alterations in the hypothalamic-pituitary-adrenal axis [3, 33, 59]

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