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These effects are thought to be mediated by the neurotrophic actions of IGF-1, which crosses the blood-brain barrier and activates neuronal survival and synaptic plasticity pathways

Under normal conditions, cortisol helps to regulate the inflammatory response, but low cortisol levels reduce the inhibition of the nuclear factor kappa B (NF-B) pathway and T lymphocyte activation, leading to a proinflammatory environment (proinflammatory cytokines such as IFN-) and immune hyperactivation (2325)

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