Lam Pok, Hong Chen-Jee, Tsai Shih-Jen
Department of Psychiatry, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan ROC.
Neurosci Lett. 2005 Apr 18;378(2):98-101. doi: 10.1016/j.neulet.2004.12.012. Epub 2004 Dec 28.
The adenosine A2a receptor (A2aAR) is thought to be implicated in the pathogenesis of panic disorder because caffeine, a potent antagonist for A2aAR, can precipitate panic attacks, and because disruption of the A2aAR gene increased anxiety-behaviors in mice. Recent studies demonstrated that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder though not by all studies. The present study tested the hypothesis that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder using a Chinese population of 104 panic disorder patients and 192 normal controls. We also tested whether the A2aAR 1976T > C polymorphism relates to the age of onset or subtype of panic disorders. Neither the distribution of the A2aAR 1976T > C genotypes (P = 0.296) or alleles (P = 0.864), nor the age of onset (P = 0.719) were significantly different among genotype groups. Furthermore, no association was demonstrated between this A2aAR polymorphism and either mitral-valve prolapse or agoraphobia in panic-disorder patients. These findings suggested that it is unlikely that the A2aAR 1976T > C polymorphism plays a major role in panic disorder pathogenesis in the Chinese population. The positive association between this polymorphism and panic disorder found in western population but not in Asian population suggests that this association could be ethnicity-dependent. The 1976C > T polymorphism may be in linkage disequilibrium with a functional variant that affects panic disorder, and the extent of this linkage disequilibrium is not similar for all ethnic populations.
腺苷A2a受体(A2aAR)被认为与惊恐障碍的发病机制有关,因为咖啡因是A2aAR的强效拮抗剂,可引发惊恐发作,而且A2aAR基因的破坏会增加小鼠的焦虑行为。最近的研究表明,A2aAR 1976T > C基因变异赋予了对惊恐障碍的易感性,不过并非所有研究都得出此结论。本研究使用104名惊恐障碍患者和192名正常对照的中国人群,检验了A2aAR 1976T > C基因变异赋予惊恐障碍易感性的假设。我们还检验了A2aAR 1976T > C多态性是否与惊恐障碍的发病年龄或亚型有关。A2aAR 1976T > C基因型(P = 0.296)或等位基因(P = 0.864)的分布,以及发病年龄(P = 0.719)在各基因型组之间均无显著差异。此外,在惊恐障碍患者中,未发现该A2aAR多态性与二尖瓣脱垂或场所恐惧症之间存在关联。这些发现表明,A2aAR 1976T > C多态性在中国人群惊恐障碍发病机制中不太可能起主要作用。在西方人群而非亚洲人群中发现的这种多态性与惊恐障碍之间的正相关表明,这种关联可能与种族有关。1976C > T多态性可能与影响惊恐障碍的功能性变异处于连锁不平衡状态,而且这种连锁不平衡的程度在所有种族人群中并不相同。