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Striatal dopamine synthesis capacity in autism spectrum disorder and its relation with social defeat: an [ 18 F]-FDOPA PET/CT study
Translational Psychiatry ( IF 5.8 ) Pub Date : 2021-01-13 , DOI: 10.1038/s41398-020-01174-w
Rik Schalbroeck 1, 2, 3 , Floris H P van Velden 3 , Lioe-Fee de Geus-Oei 3, 4 , Maqsood Yaqub 5 , Therese van Amelsvoort 2 , Jan Booij 6 , Jean-Paul Selten 1, 2
Affiliation  

Alterations in dopamine signalling have been implied in autism spectrum disorder (ASD), and these could be associated with the risk of developing a psychotic disorder in ASD adults. Negative social experiences and feelings of social defeat might result in an increase in dopamine functioning. However, few studies examined dopamine functioning in vivo in ASD. Here we examine whether striatal dopamine synthesis capacity is increased in ASD and associated with social defeat. Forty-four unmedicated, non-psychotic adults diagnosed with ASD and 22 matched controls, aged 18–30 years, completed a dynamic 3,4-dihydroxy-6-[18F]-fluoro-L-phenylalanine positron emission tomography/computed tomography ([18F]-FDOPA PET/CT) scan to measure presynaptic dopamine synthesis capacity in the striatum. We considered unwanted loneliness, ascertained using the UCLA Loneliness Scale, as primary measure of social defeat. We found no statistically significant difference in striatal dopamine synthesis capacity between ASD and controls (F1,60 = 0.026, p = 0.87). In ASD, striatal dopamine synthesis capacity was not significantly associated with loneliness (β = 0.01, p = 0.96). Secondary analyses showed comparable results when examining the associative, limbic, and sensorimotor sub-regions of the striatum (all p-values > 0.05). Results were similar before and after adjusting for age, sex, smoking-status, and PET/CT-scanner-type. In conclusion, in unmedicated, non-psychotic adults with ASD, striatal dopamine synthesis capacity is not increased and not associated with social defeat.



中文翻译:

自闭症谱系障碍纹状体多巴胺合成能力及其与社交失败的关系:[ 18 F]-FDOPA PET/CT 研究

自闭症谱系障碍 (ASD) 中暗示了多巴胺信号的改变,这些可能与 ASD 成人患精神病的风险有关。负面的社会经历和社交失败的感觉可能会导致多巴胺功能增加。然而,很少有研究检查多巴胺在 ASD 体内的功能。在这里,我们检查纹状体多巴胺合成能力是否在 ASD 中增加并与社交失败相关。44 名被诊断患有 ASD 且未接受药物治疗的非精神病成人和 22 名年龄在 18-30 岁之间的匹配对照者完成了动态 3,4-dihydroxy-6-[ 18 F]-fluoro-L-phenylalanine 正电子发射断层扫描/计算机断层扫描([ 18F]-FDOPA PET/CT) 扫描以测量纹状体中的突触前多巴胺合成能力。我们将不想要的孤独感(使用加州大学洛杉矶分校孤独感量表确定)视为社交失败的主要衡量标准。我们发现 ASD 和对照组之间的纹状体多巴胺合成能力没有统计学显着差异(F 1,60  = 0.026,p  = 0.87)。在 ASD 中,纹状体多巴胺合成能力与孤独感无显着相关性(β  = 0.01,p  = 0.96)。在检查纹状体的联想、边缘和感觉运动子区域时,二次分析显示了可比较的结果(所有p-值 > 0.05)。调整年龄、性别、吸烟状况和 PET/CT 扫描仪类型前后的结果相似。总之,在患有 ASD 的未接受药物治疗的非精神病成人中,纹状体多巴胺合成能力没有增加,并且与社交失败无关。

更新日期:2021-01-13
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