
The etiology of psychosis, particularly within the schizophrenia spectrum, is increasingly understood as a systemic neuroinflammatory event rather than solely a dopaminergic dysregulation. This paper proposes a molecular intervention strategy targeting the reduction of proinflammatory cytokines, specifically Interleukin-1β (IL-1β) and Tumor Necrosis Factor-α (TNF-α). By modulating the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, we hypothesize a significant reduction in neurotoxicity and psychotic symptomatology. We present a phytochemical protocol designed to upregulate the NRF2 antioxidant response element, thereby inhibiting the NF-κB cascade and restoring neuro-homeostasis.
Psychotic Disorders/enzymology, Psychotic Disorders/psychology, Psychotic Disorders/history, Psychotic Disorders/immunology, Psychotic Disorders, Psychotic Disorders/physiopathology, Psychotic Disorders/classification, Psychotic Disorders/complications, Psychotic Disorders/nursing, Psychotic Disorders/metabolism, Psychotic Disorders/genetics, Psychotic Disorders/diagnosis, Psychotic Disorders/economics, Psychotic Disorders/rehabilitation
Psychotic Disorders/enzymology, Psychotic Disorders/psychology, Psychotic Disorders/history, Psychotic Disorders/immunology, Psychotic Disorders, Psychotic Disorders/physiopathology, Psychotic Disorders/classification, Psychotic Disorders/complications, Psychotic Disorders/nursing, Psychotic Disorders/metabolism, Psychotic Disorders/genetics, Psychotic Disorders/diagnosis, Psychotic Disorders/economics, Psychotic Disorders/rehabilitation
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