ArticleFrontiers in psychiatry2026
Cognitive impairment and prefrontal TGF-β1 elevation in a rat model of fatigue.
Article in Frontiers in psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Chronic fatigue syndrome (CFS) is a complex disorder of unknown etiology, characterized by persistent fatigue unrelieved by rest and accompanied by cognitive dysfunction. While dysregulated cytokines are implicated in CFS pathogenesis, the role of anti-inflammatory transforming growth factor β1 (TGF-β1) remains poorly defined. Methods: This study investigated central and peripheral TGF-β1 dysregulation and cognitive function in a rat model of fatigue induced by 10-day repetitive sleep deprivation with intermittent rest. Rats were randomly divided into the control group and the fatigue group. Behavioral tests including open field test and Y-maze test were performed after the end of fatigue-loading procedure. Peripheral and central TGF-β1 levels were detected. Results: Rats in the fatigue group exhibited unchanged daytime short-term locomotor activity but significantly increased anxiety-like behavior in the open field test. In the Y-maze test, the fatigue group showed markedly reduced spontaneous alternation rates compared to controls. Furthermore, prefrontal cortical TGF-β1 levels were elevated in fatigued rats, whereas neither peripheral nor striatal TGF-β1 differed between groups. Conclusion: These findings demonstrate that the 10-day repetitive sleep deprivation with intermittent rest fatigue model induces cognitive impairment and increased anxiety-like behavior, with selective prefrontal TGF-β1 upregulation. The concomitant elevation of prefrontal TGF-β1 and cognitive deficits suggests a potential role for central TGF-β1 signaling in the pathophysiology of mental fatigue, although the precise nature of this relationship remains to be elucidated.
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