Authors : Mishti Majithia

Volume/Issue : Volume 10 - 2025, Issue 5 - May

Google Scholar : https://tinyurl.com/33836trn

DOI : https://doi.org/10.38124/ijisrt/25may1683

Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.

Abstract : Schizophrenia is a severe and chronic mental disorder characterized by profound disruptions in thinking, perception, emotions, and behavior, often leading to impaired reality testing (psychosis), social dysfunction, and cognitive deficits. This paper integrates the neurobiological perspective of schizophrenia with its genetic aspects. While dopamine dysregulation has long been implicated in its pathology, emerging research has emphasized the critical role of glutamatergic neurotransmission. The dopamine hypothesis is one of the primary theories proposed for the development of schizophrenia, as it was found that typical antipsychotics function by blocking dopamine D2 receptors. However, this hypothesis was not able to fully explain the cognitive and negative symptoms of schizophrenia. Thus, a new hypothesis was formed, called the glutamate hypothesis, which postulates that schizophrenia results from the hypofunction of the glutamatergic system, especially by blocking NMDA receptors. Genetic studies have identified several susceptibility genes involved in glutamatergic regulation, including G72 (DAOA), DTNBP1 (dysbindin), GRM3, and NRG1, which modulate synaptic glutamate signaling and receptor function. Understanding these genetic influences provides a more integrative view of the neurobiological mechanisms of schizophrenia, and opens new avenues for targeted treatment strategies beyond the dopaminergic model.

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