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自闭症谱系障碍中社会和认知障碍与生物标志物的关联。

Association of social and cognitive impairment and biomarkers in autism spectrum disorders.

机构信息

Biochemistry Department, Science College, King Saud University, P,O box 22452, Zip code 11495 Riyadh, Saudi Arabia.

出版信息

J Neuroinflammation. 2014 Jan 8;11:4. doi: 10.1186/1742-2094-11-4.

Abstract

OBJECTIVES

The neurological basis for autism is still not fully understood, and the role of the interaction between neuro-inflammation and neurotransmission impairment needs to be clearer. This study aims to test the possible association between impaired levels of gamma aminobutyric acid (GABA), serotonin, dopamine, oxytocin, and interferon-γ-induced protein-16 (IFI16) and the severity of social and cognitive dysfunctions in individuals with autism spectrum disorders.

MATERIALS AND METHODS

GABA, serotonin, dopamine, oxytocin, and IFI16 as biochemical parameters related to neurochemistry and inflammation were determined in the plasma of 52 Saudi autistic male patients, categorized as mild-moderate and severe as indicated by their Childhood Autism Rating Scale (CARS) or social responsiveness scale (SRS), and compared to 30 age- and gender-matched control samples.

RESULTS

The data indicated that Saudi patients with autism have remarkably impaired plasma levels of the measured parameters compared to age and gender-matched controls. While serotonin in platelet-free plasma and dopamine did not correlated with the severity in social and cognitive dysfunction, GABA, oxytocin, and IFI16 were remarkably associated with the severity of both tested scores (SRS and CARS).

CONCLUSIONS

The relationship between the selected parameters confirms the role of impaired neurochemistry and neuro-inflammation in the etiology of autism spectrum disorders and the possibility of using GABA, oxytocin, and IFI16 as markers of autism severity. Receiver operating characteristic analysis together with predictiveness diagrams proved that the measured parameters could be used as predictive biomarkers of clinical symptoms and provide significant guidance for future therapeutic strategy to re-establish physiological homeostasis.

摘要

目的

自闭症的神经基础仍不完全清楚,需要更清楚地了解神经炎症与神经传递损伤之间的相互作用的作用。本研究旨在测试自闭症谱系障碍个体中γ-氨基丁酸(GABA)、血清素、多巴胺、催产素和干扰素-γ诱导蛋白-16(IFI16)水平受损与社会和认知功能障碍严重程度之间的可能关联。

材料和方法

在 52 名沙特自闭症男性患者的血浆中确定了与神经化学和炎症相关的 GABA、血清素、多巴胺、催产素和 IFI16 等生化参数,根据他们的儿童自闭症评定量表(CARS)或社会反应量表(SRS)分为轻度-中度和重度,并与 30 名年龄和性别匹配的对照组进行比较。

结果

数据表明,与年龄和性别匹配的对照组相比,自闭症沙特患者的血浆中这些参数的水平明显受损。虽然血小板游离血浆中的血清素和多巴胺与社会和认知功能障碍的严重程度无关,但 GABA、催产素和 IFI16 与两种测试评分(SRS 和 CARS)的严重程度明显相关。

结论

所选参数之间的关系证实了神经化学和神经炎症受损在自闭症谱系障碍发病机制中的作用,以及使用 GABA、催产素和 IFI16 作为自闭症严重程度标志物的可能性。接收器操作特性分析和预测图证明,所测量的参数可用作临床症状的预测生物标志物,并为未来重建生理平衡的治疗策略提供重要指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e242/3896747/80f969a046d3/1742-2094-11-4-1.jpg

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