Schizophrenia is a multifaceted neuropsychiatric condition marked by a diverse array of symptoms, which can be categorized into positive, negative, and cognitive deficits. The underlying pathophysiology of this disorder is complex, involving a variety of mechanisms such as the dysregulation of neurotransmitter systems, neuroinflammatory responses, and neuronal dysfunction induced by oxidative stress. These interrelated processes lead to synaptic and neuronal impairments, which ultimately result in the clinical manifestations observed in patients with schizophrenia. The challenge of elucidating the molecular mechanisms that contribute to schizophrenia is significant, given the disorder's intricate and multifactorial characteristics. Neuroinflammatory pathways, such as those involving NF-κB, MAPK/ERK, kynurenine pathway and the activation of the NLRP3 inflammasome, play a significant role in promoting oxidative stress, synaptic dysfunction, and neuronal injury, which in turn aggravate cognitive and negative symptoms associated with schizophrenia. Although current pharmacological treatments primarily focus on dopamine and glutamate systems, their limited effectiveness in alleviating cognitive and negative symptoms highlights the necessity for a deeper mechanistic understanding of the disorder at the molecular level. Progress in neurobiological research, particularly concerning inflammatory pathways, mitochondrial dysfunction, and synaptic plasticity, is essential for the development of more targeted and effective therapeutic strategies for schizophrenia. This review underscores the critical need for a deeper understanding of molecular insights and treatment methodologies in the context of schizophrenia.
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