Humanistic Studies and Social Researches

Abstract Background: Schizophrenia is a severe psychiatric disorder characterized by a complex, multifactorial origin. While dopaminergic theories have been predominant, contemporary perspectives highlight an integrated dysfunction across genetic, molecular, and neural circuit levels, rooted in neurodevelopmental abnormalities.
Objectives: This review synthesizes recent evidence from genetics, neuroimaging, and molecular psychiatry to present an updated model of schizophrenia pathophysiology. It focuses on the interplay between synaptic pruning, interneuron dysfunction, and brain network dysconnectivity.
Methods: We conducted a narrative, integrative review. Searches in PubMed, Scopus, and Web of Science (2014-2025) utilized terms like "schizophrenia neurobiology," "dysconnectivity," "NMDA receptor hypofunction," "parvalbumin interneurons," and "genetic risk." Evidence was thematically synthesized to construct a coherent pathophysiological model.
Results: Findings outline a pathway from genetic risk (e.g., complement C4 loci) to excessive adolescent synaptic pruning, leading to impairment of parvalbumin-positive GABAergic interneurons. This results in N-methyl-D-aspartate receptor (NMDAR) hypofunction, a disrupted cortical excitation/inhibition balance, and aberrant neural oscillations. These local deficits manifest as large-scale dysconnectivity within cortico-striato-thalamo-cortical (CSTC) circuits, underpinning positive, negative, and cognitive symptoms. Dopaminergic dysregulation is positioned downstream of primary glutamatergic/GABAergic pathology.
Conclusion: Schizophrenia is best conceptualized as a neurodevelopmental disorder of synaptic connectivity. Future therapeutics should target earlier pathological stages, such as immune-mediated pruning and glutamatergic signalling, offering potential for novel treatments and preventative strategies.

Abstract Background: Although oncology traditionally emphasizes survival rates, the patient's journey is deeply influenced by their subjective experience and psychological state. Continuity of Care (CoC)—the consistent, coordinated, and unified management of care over time—is increasingly recognized as a vital element that extends beyond its possible effects on mortality.
Objective: This review consolidates current research to explore how CoC affects patient-reported experience measures (PREMs) and mental health results in individuals with cancer.
Methods: A systematic search of databases (including PubMed, PsycINFO, CINAHL) was performed for studies published from 2000 to 2024. Search terms comprised "continuity of care," "cancer," "oncology," "patient experience," "quality of life," "anxiety," "depression," "care coordination," and "therapeutic alliance."
results: Substantial evidence shows that greater CoC is reliably linked to better patient experiences, including enhanced communication, trust, and security. Additionally, CoC serves as an important protective factor against psychological illness, lowering anxiety, depression, and sensations of abandonment, especially during care transitions and survivorship.
Conclusion: CoC is a core, adjustable component of quality cancer care that directly improves patients' care experiences and protects their mental health. Emphasizing CoC through intentional models and policies is crucial for realizing genuinely patient-focused oncology.