The article appears on bioRxiv under DOI https://doi.org/10.64898/2026.10.11.758339 and is explicitly labeled as a preprint that has not been peer reviewed. The author list—led by Ziguo Lan and including investigators from Kyoto University, Shiga University of Medical Science, RIKEN, Johns Hopkins and other institutions—is presented in full in the supplied extract. Affiliations and author names are concrete; the source fragment supplies these bibliographic elements but stops short of study details.
The title reports that investigators developed a novel DISC1-perturbed monkey model and examined adolescent prodromal phenotypes relevant to psychiatric disorders. That claim, as written in the preprint title, signals the study’s focus on early-stage (adolescent, prodromal) manifestations in a nonhuman primate genetic perturbation model. The supplied portion of the source confirms the title and authorship but does not provide specific descriptions of observed phenotypes, endpoints, or assays.
The text fragment provided for this rewrite lacks critical methodological and results information. The source did not report, within the excerpt delivered here, any of the following: the experimental design, the technique used to perturb DISC1, the number or ages of animals studied, control groups, behavioral batteries used, neuroimaging sequences, histological or molecular readouts, predefined primary or secondary endpoints, or statistical outcomes. The supplied content also did not include safety, welfare, or ethical oversight statements beyond author affiliations. Because those elements are absent from the provided extract, no factual reconstruction of methods or findings can be made from this material alone.
Readers of the supplied excerpt cannot determine which adolescent prodromal features were studied, how reproducible the effects were, or whether the observed signals—if any—map onto specific psychiatric diagnoses. The preprint fragment does not specify whether the study team observed behavioral changes, cognitive deficits, social alterations, neuroanatomical differences, molecular pathway shifts, or combinations of these. The extract also omits data on effect magnitude, variability, and statistical significance. These omissions leave several practical questions unresolved for clinicians and researchers: what experimental approach was used to perturb DISC1 in primates; what phenotypes emerged and at what developmental time points; what outcome measures were prioritized; and how the authors interpret the translational relevance.
The supplied material provides the DOI and full author list, enabling direct retrieval of the preprint on bioRxiv for readers who want the complete report. For professionals evaluating the model’s utility, the following actions are necessary and supported by the source metadata: access the full preprint via the DOI to review methods and results; assess whether the authors report animal numbers, blinding, and controls; examine the behavioral, imaging, and molecular datasets as presented; and note that the preprint status means findings are provisional until peer review is completed.
Limitations noted here derive from the content provided to this rewrite. The supplied extract contains bibliographic and authorship information and the preprint label, but it does not include experimental methods, quantitative findings, endpoints, or conclusions. Any interpretation beyond the presence of a DISC1-perturbed monkey model and the claim of adolescent prodromal phenotypes would require consulting the full preprint text available via the DOI.
Readers and clinicians who require detailed evidence for translational or clinical decision-making should retrieve the complete manuscript and track its peer-review status. The bioRxiv record and DOI listed in the supplied extract are the appropriate, documented starting points for that follow-up. The supplied excerpt does not report subsequent regulatory milestones, peer-review outcomes, or next-step experiments; those items are therefore outside the scope of this rewrite based solely on the provided source material.