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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on the other hand, bone-derived cells and metabolites are capable of crossing the BBB, thereby providing sustained immune regulation and neuroprotection
Resistance to trophic neurite outgrowth of sensory neurons exposed to insulin