Role of Neurochemicals in Schizophrenia

(E-pub Ahead of Print)

Author(s): Sher Singh, Deepa Khanna*, Sanjeev Kalra.

Journal Name: Current Psychopharmacology

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Abstract:

Background: Schizophrenia is a complex, unpredictable and severe psychiatric disorder, which affects several domains of cognition, behavior and characterized by positive, negative, and cognitive symptoms. Etiology of schizophrenia represent involvement of environmental factors, role of genes, social stressors, like discrimination or economic hardship, relationships, childhood difficulty, use of cannabis in adolescence, maternal stress, nutritional deficiencies, maternal infections, intrauterine growth retardation, and complications of pregnancy, while pathophysiology represents dysfunctional neurotransmission of dopamine, stress-associated signaling cascades (Gabanergic, glutamatergic, cholinergic, serotonin, adrenergic singling cascades) and enzymatic changes (acetylcholinesterase, catechol-o-methyl-transferase, monoamine oxidase, phosphodiesterase).

Objective: The objective of the current review is to determine the role of pathophysiological hypothesis impairments leading to positive, negative and cognitive symptoms of schizophrenia.

Methods: Various pathophysiological hypothesis of schizophrenia were identified through searching relevant databases including: PubMed, Scopus, and Web of Science up to 2019, using the keywords ‘schizophrenia, role of dopamine, acetylcholine, oxidative stress, inflammation in schizophrenia.

Result: Alterations in neurotransmission of dopamine, stress-associated signaling cascades (Gabanergic, glutamatergic, cholinergic, serotonin, adrenergic singling cascades) and enzymatic changes (acetylcholinesterase, catechol-o-methyl-transferase, monoamine oxidase, phosphodiesterase were compiled in this review for easy learning of Schizophrenia.

Keywords: Schizophrenia, Symptoms, Pathophysiology, dopamine, GABA, acetylcholine, oxidative stress, neuro-inflammation and mitochondrial dysfunctioning.

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Article Details

(E-pub Ahead of Print)
DOI: 10.2174/2211556009666200401150756