ArticleSchizophrenia bulletin2026
Autophagy in Schizophrenia: A Continuum From Developmental Vulnerability to Progressive Neuronal Stress? A Scoping Review.
Article in Schizophrenia bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- mTOR-driven autophagy-inflammation crosstalk underlies schizophrenia pathophysiology.Translational psychiatry · 2026Article
- Neuroimaging evidence of mitochondrial dysfunction and inflammation in psychiatric disorders: a review.Psychoradiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
background and hypothesisAutophagy, the cell's primary degradation and recycling system, is essential for neuronal homeostasis. A structured synthesis of studies directly investigating autophagy in schizophrenia (SCZ) is lacking. This scoping review aimed to map the available evidence directly assessing autophagy processes in SCZ. STUDY
designWe systematically searched Medline (via Ovid), Embase, and PsycINFO from inception to February 2025. Twenty-four eligible studies-encompassing clinical cohorts, postmortem brain tissue, animal and cellular SCZ-relevant models-were thematically analyzed. STUDY
resultsFindings indicated impaired autophagy in SCZ, implicating it in 3 main processes: (1) disrupted neurodevelopment/synaptic pruning, (2) lysosomal dysfunction/proteostasis, (3) compromised mitochondrial turnover/metabolic homeostasis. Antipsychotic treatment showed variable effects, with some agents partially restoring autophagic markers, whereas others heightened dysfunction. Transcriptomic studies identified autophagy-related gene signatures with potential diagnostic relevance. Synthesizing these findings, impaired autophagy emerged as a possible mechanistic link between early neurodevelopmental vulnerability and progressive cellular stress, which may underlie disease progression in some cases.
conclusionsAutophagy 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.