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Increased ratio of mature BDNF to precursor-BDNF in patients with major depressive disorder with severe anhedonia.
Journal of Psychiatric Research ( IF 4.8 ) Pub Date : 2020-05-12 , DOI: 10.1016/j.jpsychires.2020.05.010
Congchong Wu 1 , Jing Lu 2 , Shaojia Lu 2 , Manli Huang 2 , Yi Xu 2
Affiliation  

BACKGROUND Although studies have shown that severe anhedonia in patients with major depressive disorder (MDD) is associated with poor treatment outcomes, the biological mechanism of this feature is unclear. The aim of this study was to investigate the dysfunction of brain-derived neurotrophic factor (BDNF) metabolism, measured by the ratio of mature BDNF to precursor-BDNF, in MDD patients with severe anhedonia. METHODS We measured plasma levels of mature BDNF (mBDNF), precursor-BDNF (proBDNF), tissue plasminogen activator (tPA) and tropomyosin-related kinase B (trkB) in outpatients with MDD with anhedonia (n = 26), outpatients with MDD without anhedonia (n = 29) and age- and sex-matched healthy controls (HCs, n = 38) by enzyme-linked immunosorbent assay kits, and we calculated the ratio of mBDNF to proBDNF (M/P). We compared these biological determinants among the three groups and explored the interrelationships between anhedonia severity and BDNF metabolism. RESULTS The levels of mBDNF, proBDNF, and tPA and the ratio of M/P were identified with highly significant differences among the three groups. Compared with MDD patients without anhedonia and healthy controls, MDD patients with anhedonia showed higher level of the ratio of M/P, and it was positively associated with the SHAPS scores in MDD patients. Compared to healthy controls, the plasma tPA concentrations were higher in MDD patients with anhedonia but were not different from those in MDD patients without anhedonia. CONCLUSION These results provide novel evidence regarding the relationship between anhedonia and plasma BDNF metabolism. The hypermetabolism of BDNF may be a function of anhedonia rather than other characteristics in MDD.

中文翻译:

在患有严重快感缺失的重度抑郁症患者中,成熟 BDNF 与前体 BDNF 的比率增加。

背景 尽管研究表明重度抑郁症 (MDD) 患者的严重快感缺失与不良治疗结果相关,但该特征的生物学机制尚不清楚。本研究的目的是调查患有严重快感缺失的 MDD 患者的脑源性神经营养因子 (BDNF) 代谢功能障碍,通过成熟 BDNF 与前体-BDNF 的比率来衡量。方法 我们测量了患有快感缺失的 MDD 门诊患者 (n = 26) 和没有 MDD 的门诊患者的成熟 BDNF (mBDNF)、前体-BDNF (proBDNF)、组织纤溶酶原激活物 (tPA) 和原肌球蛋白相关激酶 B (trkB) 的血浆水平。通过酶联免疫吸附测定试剂盒检测快感缺失(n = 29)和年龄和性别匹配的健康对照(HCs,n = 38),我们计算了 mBDNF 与 proBDNF 的比率(M/P)。我们比较了三组之间的这些生物学决定因素,并探讨了快感缺失严重程度与 BDNF 代谢之间的相互关系。结果三组间mBDNF、proBDNF、tPA水平及M/P比值均具有极显着性差异。与无快感缺失的MDD患者和健康对照组相比,伴有快感缺失的MDD患者M/P比值水平较高,且与MDD患者SHAPS评分呈正相关。与健康对照组相比,伴有快感缺失的 MDD 患者血浆 tPA 浓度较高,但与没有快感缺失的 MDD 患者无差异。结论 这些结果为快感缺乏和血浆 BDNF 代谢之间的关系提供了新的证据。
更新日期:2020-05-12
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