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Its pathophysiology involves multiple interconnected mechanisms, including monoaminergic neurotransmitter depletion, impaired neurotrophic signaling, neuroinflammation accompanied by hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and glutamate-induced excitotoxicity (Medeir et al., 2020)

human evidence is limited, the combination is unstudied, and individual results vary

Their investigation of a transgenic mouse model (Gpx5-/-) revealed that oxidative DNA damage does not disrupt the organization of chromosomes but significantly alters specific 3D nuclear parameters

Inflammatory factors stimulate increased brain microvascular permeability, such as IL-1, TNF-, and IL-6