生物谷報道：抑郁癥是困繞當(dāng)代社會的重大的疾病,，雖然神經(jīng)科學(xué)工作者研究了很多年，但是其機(jī)理一直不明朗,。既往的研究認(rèn)為5-HT系統(tǒng)失調(diào)可能是其關(guān)鍵因素，但為什么會失調(diào)，其分子背景并不清楚,。
將于2005年1月出版的Neuron上將刊登華人學(xué)者張曉東的一篇最新研究成果，hTPH2基因可能是關(guān)鍵基因,。這個基因直接影響了5-HT的合成,，從而與抑郁相關(guān)。他們采用了分析該基因的SNP,，以及通過loss of function的方法證實了這一基因的關(guān)鍵性作用,。下面的摘要，全文（PDF）提供下載,。
Dysregulation of central serotonin neurotransmission has been widely suspected as an important contributor to major depression. Here, we identify a (G1463A) single nucleotide polymorphism (SNP) in the rate-limiting enzyme of neuronal serotonin synthesis, human tryptophan hydroxylase-2 (hTPH2). The functional SNP in hTPH2 replaces the highly conserved Arg441 with His, which results in ∼80% loss of function in serotonin production when hTPH2 is expressed in PC12 cells. Strikingly, SNP analysis in a cohort of 87 patients with unipolar major depression revealed that nine patients carried the mutant (1463A) allele, while among 219 controls, three subjects carried this mutation. In addition, this functional SNP was not found in a cohort of 60 bipolar disorder patients. Identification of a loss-of-function mutation in hTPH2 suggests that defect in brain serotonin synthesis may represent an important risk factor for unipolar major depression
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