Autophagy in Schizophrenia: A Continuum From Developmental Vulnerability to Progressive Neuronal Stress? A Scoping Review

Autophagy dysfunction may contribute to both early neurodevelopmental and later progressive cellular changes in SCZ. However, much of the current evidence derives from cross-sectional studies, peripheral biomarkers or animal models, with limited direct evidence from the human central nervous system. These limitations constrain causal interpretation. Even so, autophagy represents a promising therapeutic target, with potential to support early neural development and prevent progressive cellular decline. Longitudinal, multimodal studies integrating peripheral and central autophagy markers with clinical outcomes are needed to clarify autophagy's role in SCZ pathophysiology and treatment.