Attenuated PER3 amplitude in hair follicles is associated with sleep irregularity in schizophrenia.

IF 7.5 1区 医学 Q1 PSYCHIATRY
Mikkel E I Kolind, Rikke Kruse, Jan C Brønd, Afsaneh M Nejad, Lasse K Bak, Charlotte S Larsen, Kurt Højlund, Christoph P Beier, Elsebeth Stenager, Claus B Juhl
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Abstract

Circadian dysregulation is prevalent in both schizophrenia and obesity, yet the molecular mechanisms underpinning these disturbances remain unclear. We examined circadian variation in clock gene expression using repeated hair follicle self-sampling across two days in 66 adults: 22 with schizophrenia and obesity (SCH-OB), 22 with obesity but no psychiatric disorder (OB), and 22 normal-weight controls (LEAN). Gene expression was quantified by qPCR, and complementary markers included salivary cortisol and melatonin, oral pH and temperature, and accelerometer-derived sleep metrics. Evidence of rhythmic expression was detected in five of six clock genes. PER3 amplitude was significantly reduced in SCH-OB compared with both OB and LEAN (p < 0.01) and correlated positively with sleep regularity (p = 0.006). Cortisol rhythms were preserved across groups, whereas melatonin amplitude was attenuated in SCH-OB relative to LEAN (p < 0.05). Hair follicle sampling proved highly feasible, with >98% compliance. These findings indicate that individuals with schizophrenia exhibit dampened circadian rhythms in PER3 expression that parallel irregular sleep patterns, supporting hair follicle-based sampling as a practical tool for assessing molecular rhythm parameters in real-world conditions.

毛囊PER3振幅减弱与精神分裂症患者睡眠不规律有关。
昼夜节律失调在精神分裂症和肥胖症中都很普遍,但支持这些紊乱的分子机制尚不清楚。我们对66名成年人进行了为期两天的重复毛囊自我采样,研究了生物钟基因表达的昼夜变化:22名患有精神分裂症和肥胖症(SCH-OB), 22名患有肥胖症但没有精神疾病(OB), 22名体重正常的对照组(LEAN)。通过qPCR量化基因表达,补充标记包括唾液皮质醇和褪黑激素,口腔pH和温度,以及加速度计衍生的睡眠指标。在6个时钟基因中的5个中检测到节律性表达的证据。与OB和LEAN相比,SCH-OB的PER3振幅显著降低(p < 98%)。这些发现表明,精神分裂症患者在PER3表达中表现出抑制的昼夜节律,与不规则的睡眠模式相似,支持基于毛囊的采样作为评估现实条件下分子节律参数的实用工具。
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来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
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