 Scientists say they've identified a flawed gene that appears to promote manic-depression, or bipolar disorder, a finding that could eventually help guide scientists to new treatments.
A particular variant of the gene was associated with only about 3 percent of cases in a study, but researchers said other variants might be involved with more. Follow-up research might help reveal the mysterious underlying biology that makes some people susceptible to the disorder, and so help scientists devise new treatments, said the study's senior author, Dr. John Kelsoe of the University of California, San Diego. The work is reported in Monday's issue of the journal Molecular Psychiatry. Previous studies have suggested that other genes are involved in manic-depression. But one expert, Dr. Melvin McInnis of Johns Hopkins University in Baltimore, said in an interview that he thinks Kelsoe's new work and another recent study provide the strongest evidence for involvement of particular genes in the disease. Manic-depression, which affects about 2.3 million American adults, involves episodes of depression and mania, states of abnormally high mood or irritability. While effective treatment is available, scientists would like to find better medications. Genetics clearly play a role. Kelsoe's work focused on a gene called GRK3, which influences the brain's sensitivity to chemical messages brain cells send each other. Defects in the gene might promote manic-depression by making people oversensitive to these messages, which are carried by dopamine and other substances, he said. Kelsoe and colleagues found statistical evidence tying a particular variant of the GRK3 gene to the disease. They tracked the inheritance of this variant from parent to child in families with a history of bipolar disorder. Overall, the variant was passed along more often than one would expect by chance to a child who later developed the disease. That suggests the variant promotes susceptibility to bipolar disorder. The association between the variant gene and the disorder appeared in one group of 153 families and a second group of 275 families. That association is only statistical, and Kelsoe said researchers now are looking for biological evidence that this variant of the gene acts abnormally.
(Agencies) | 科學(xué)家稱他們已經(jīng)發(fā)現(xiàn)了一種引發(fā)躁郁癥，或稱雙極性疾患的破壞性基因。這項發(fā)現(xiàn)可以最終在躁郁癥的治療方面為科學(xué)家們提供指導(dǎo)性幫助。 研究者們在研究中發(fā)現(xiàn)，僅有3％的病例證實是和此種基因的一種特殊變體有關(guān)，但是其他的變體的誘病率可能會更高。 這項研究報告的作者，圣地亞哥的加利福尼亞大學(xué)的約翰·凱爾索博士說，今后的深入研究或許可以揭示這種神秘的隱形生物是如何讓某些人患上躁郁癥的，這樣就可以幫助科學(xué)家們制定出新的治療方案。 這項研究刊登在了6月16日的期刊《分子精神病學(xué)》上。 從前的研究發(fā)現(xiàn)有其他種類的基因同躁郁癥的發(fā)病有關(guān)。但是位于巴爾的摩的約翰斯·霍普金斯大學(xué)的梅爾文·麥金尼斯博士，一位研究躁郁癥的專家在一次采訪中說，他認(rèn)為凱爾索博士的新研究和近期的其他有關(guān)研究都有力地證明這種病同某種特殊的基因有關(guān)。 目前美國有230萬成年人飽受躁郁癥之苦。這種病的癥候主要是間歇性的抑郁和狂躁，出現(xiàn)反常的情緒高漲或者興奮。 盡管我們現(xiàn)在已經(jīng)有了有效的治療方法，但是科學(xué)家們還在尋求更好的治療途徑。 研究表明，遺傳學(xué)顯然同這種病有關(guān)。凱爾索博士的研究集中在一種成為GRK3的基因上。這種基因影響大腦對化學(xué)成分和大腦細(xì)胞之間相互傳遞的敏感度。凱爾索博士說，這種基因的特性可以最終造成人們對這些成分（通常在多巴胺和其他物質(zhì)中）的過分敏感，而誘發(fā)躁郁癥。 凱爾索博士和同事們已經(jīng)發(fā)現(xiàn)了同GRK3這種特殊基因變體相關(guān)的數(shù)據(jù)證據(jù)。他們跟蹤研究了有躁郁癥病史的家庭中帶有這種變體的父母和孩子之間的遺傳情況?？偟膩碚f，這種變體通常是會由父母遺傳給孩子的，而孩子日后自然也會患上躁郁癥。 這就說明正是這種變體誘發(fā)了躁郁癥。 這種基因變體和躁郁癥之間的研究結(jié)果是在分別對153個家庭和275個家庭進行調(diào)查之后得出的。但是目前這個結(jié)果還只停留在數(shù)據(jù)階段，因此凱爾索博士說研究者們正在尋找證明這種基因變體反常作用的生物學(xué)方面的證據(jù)。
譯者注：
1. 所謂"躁郁癥"（manic-depression），一般而言是指個體有時出現(xiàn)抑郁的癥狀，有時又出現(xiàn)狂躁的癥狀，此兩種特征不斷的交互出現(xiàn)之情形，因此又稱之為雙極性疾患（bipolar disorder），也就是說個體會出現(xiàn)兩極的情緒反應(yīng)，一為狂躁，另一為抑郁。當(dāng)個體在狂躁階段，其出現(xiàn)的特征為情緒異常興奮、自我膨脹，睡眠時數(shù)減少，非常健談、多話，常常是滔滔不絕講個沒完，另外他們的思考或想法也經(jīng)常跳來跳去，稱之為跳躍性思考（flight of ideas），易分心，在行為上我們可以看到其常常瘋狂購物，而不管價錢多少等失控行為特征。當(dāng)個體處于抑郁的階段，其特征又顯示出心情沮喪低沈、對任何事缺乏反應(yīng)或興趣、體重改變、產(chǎn)生睡眠困擾、缺乏活力、負(fù)向的認(rèn)知或看法等等的特征。
2. 多巴胺：一種治療腦神經(jīng)病的藥物
(中國日報網(wǎng)站譯) |
Updated: 2003-06-17 01:00
