Neurocognitive Impairment Profiles and Cortical Dysregulation in Schizophrenia Spectrum Disorders

Abstract

Schizophrenia spectrum disorders (SSDs) are severe neuropsychiatric conditions characterized not only by positive and negative symptoms but also by profound neurocognitive impairments that significantly affect functional recovery and quality of life. This review paper examines the neurocognitive impairment profiles and cortical dysregulation mechanisms underlying SSDs, with emphasis on the interaction between cognitive dysfunction, large-scale brain network abnormalities, and neurochemical disturbances. The study explores the stratified continuum of cognitive impairment across healthy individuals, first-degree relatives, clinical high-risk populations, first-episode psychosis, and chronic schizophrenia patients. Core cognitive deficits including processing speed, working memory, executive function, attention, verbal learning, and social cognition are critically analyzed in relation to their impact on daily functioning and psychosocial outcomes. The review further highlights the role of the triple network model involving the Salience Network (SN), Default Mode Network (DMN), and Central Executive Network (CEN), whose dysregulation contributes to impaired cognitive control and abnormal information processing in schizophrenia. Cellular mechanisms such as dendritic spine loss, excessive synaptic pruning, GABAergic interneuron dysfunction, and excitation-inhibition imbalance are discussed alongside neurochemical abnormalities involving dopamine, glutamate, and GABA systems. Additionally, computational psychiatry approaches and predictive coding frameworks are examined to explain aberrant salience and impaired reality processing. Emerging therapeutic interventions including cognitive remediation, virtual reality-based therapies, repetitive transcranial magnetic stimulation (rTMS), magnetic seizure therapy (MST), and artificial intelligence-assisted rehabilitation are also reviewed. Overall, this paper emphasizes that neurocognitive dysfunction and cortical dysregulation represent central pathophysiological features of SSDs and critical targets for future personalized therapeutic strategies.