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高智商、抑郁、注意力缺陷和自閉的基因都找到了

高智商、抑郁、注意力缺陷和自閉的基因都找到了

GLENN FLEISHMAN 2018年07月02日
具有高智商基因優(yōu)勢(shì)的人壽命可能更長,但也可能會(huì)出現(xiàn)自閉癥狀。

祖源和DNA測(cè)試網(wǎng)站MyHeritage(我的遺傳)成立了專用服務(wù)器,存儲(chǔ)了9200萬用戶的賬號(hào)郵箱地址和哈希密碼。圖:Alfred Pasieka—Getty Images/Science Photo Library

《自然基因》(Nature Genetics)6月25日發(fā)表的兩項(xiàng)研究稱,高智商和幸福感由1000種基因控制——只占全部基因的4%——引發(fā)抑郁、焦慮、精神分裂的基因種類甚至更少。具有高智商基因優(yōu)勢(shì)的人壽命可能更長,但也可能會(huì)出現(xiàn)自閉癥狀。

利用該研究,可以更好地診斷自閉癥、注意力缺乏障礙癥,識(shí)別可能患上阿茲海默綜合癥的人。此外,通過了解這些基因,我們可以使用基因療法修改基因直接治療有關(guān)病癥或者減患病風(fēng)險(xiǎn),目前基因療法對(duì)某些疾病的治療正處于臨床測(cè)試階段。

因?yàn)樯鲜鲅芯堪l(fā)現(xiàn)了決定智商的潛在機(jī)制,可能會(huì)引發(fā)人們對(duì)基因造成智力差異以及是否允許有條件的人接受治療獲得壽命產(chǎn)生爭議。這項(xiàng)研究不分種族、民族、性別或其他類似因素,然而人們短期內(nèi)上沒有能力通過調(diào)整一長串基因改變?nèi)祟悺?

此前的研究表明,智商高低及患上抑郁和其它神經(jīng)質(zhì)的風(fēng)險(xiǎn)都是可遺傳的。但是基因的作用機(jī)制仍不明晰,雖然越來越多的致病基因被發(fā)現(xiàn)。

上述兩項(xiàng)研究為我們查明哪些基因可以影響日常行為和智力成就提供了重要方向。

神經(jīng)質(zhì)被認(rèn)為可能會(huì)導(dǎo)致抑郁、焦慮、精神分裂等一系列問題,降低生活質(zhì)量。歐洲、美國和23andMe公司對(duì)神經(jīng)質(zhì)進(jìn)行了研究,分析了近45萬人的基因特點(diǎn)及問卷調(diào)查結(jié)果,發(fā)現(xiàn)近600種基因、136個(gè)基因染色體區(qū)域(基因位點(diǎn))和神經(jīng)質(zhì)有很大關(guān)系。研究還發(fā)現(xiàn),抑郁和焦慮的路徑可能不同。

阿姆斯特丹自由大學(xué)的丹尼爾·普斯特胡瑪還進(jìn)行了另外一項(xiàng)研究,參與該項(xiàng)目的研究人員和機(jī)構(gòu)數(shù)量更多,遍布世界各地。研究分析了30萬人的數(shù)據(jù),探尋基因與智商間的關(guān)系,發(fā)現(xiàn)1016種基因、205個(gè)點(diǎn)位都和智商有關(guān),并且有利于降低某些疾病的患病風(fēng)險(xiǎn),其中絕大多數(shù)基因都是新發(fā)現(xiàn)。

這些疾病包括阿茲海默綜合癥和注意力缺陷障礙癥。上述研究還表明,智商越高可能意味著壽命越長,但也越容易孤僻。

這兩項(xiàng)新研究的完成有賴于越來越多的人進(jìn)行族譜分析,這種基因分析研究的是基因特點(diǎn)而非完整的基因序列。全球已經(jīng)有幾十萬人同意將他們的基因數(shù)據(jù)、對(duì)應(yīng)的健康信息、問卷調(diào)查和認(rèn)知測(cè)試用于研究。然而這些研究數(shù)據(jù)幾乎都來自于美國和少數(shù)歐洲國家的人。

薈萃分析需要將多個(gè)相近研究的數(shù)據(jù)重新進(jìn)行檢查,利用統(tǒng)計(jì)方法去除錯(cuò)誤、強(qiáng)化主要結(jié)論。因此通過薈萃分析,有時(shí)會(huì)發(fā)現(xiàn)一組研究結(jié)果相互沖突,有時(shí)會(huì)得出更加縝密的結(jié)論。

這兩項(xiàng)研究并未提出確鑿的結(jié)論,但是為未來研究提供了重要指導(dǎo),能夠?qū)?shù)據(jù)分析進(jìn)行更直接的配對(duì)和分析。(財(cái)富中文網(wǎng))

譯者:Agatha?

Intelligence and a sense of well-being may result from just over 1,000 of our genes—as little as 4% of our genome—while depression, anxiety, and schizophrenia could be caused by even fewer, according to two studies published in Nature Genetics on June 25.

People with genetic advantages towards intelligence may live longer, too, but also be more likely to have symptoms associated with autism.

The impact of this research could be better diagnoses of autism and ADHD, and of people at risk for depression, Alzheimer’s, and schizophrenia. Beyond diagnosis, a better understand of these genes could allow direct treatment for—or the reduction of risk of developing—diseases or psychiatric traits through gene therapy, a method of directly modifying genes that is proving itself in clinical testing for particular conditions.

Because the research reveals underlying mechanisms that contribute to intelligence, it could help fuel controversies about genetically based differences in intelligence, as well as whether to allow those who could afford it to receive therapy that might let them live longer. This study didn’t look into race, ethnicity, gender, or similar factors, however, and the ability to manipulate a large set of genes to change humans isn’t on the horizon.

Previous research has shown that both above- and below-average intelligenceand a risk for depression and other aspects of neuroticism can be inherited. But the genetic mechanisms have remained murky, even as ever more genes that contribute to a variety of physical diseases have been mapped.

These two studies provide significant direction in identifying the genes that can affect everyday behavior and intellectual achievement.

One study examined neuroticism, considered a risk factor for a host of traits that can degrade the quality of life, including depression, anxiety, and schizophrenia. Examining genetic traits and surveys from nearly 450,000 people, researchers in Europe and the U.S., and from the company 23andMe found almost 600 genes and 136 regions on chromosomes (“genomic loci”) that have significant correlations with those aspects of neuroticism. Depression and worry seemed to have different pathways, the study found.

The other study, which shared as corresponding author, Danielle Posthuma of Vrije Universiteit Amsterdam, and had an even larger array of researchers and institutions working around the world, examined data from just under 300,000 people to draw connections on intelligence. The study found 1,016 genes and 205 locations, nearly all of them previously unconnected with intelligence, had a correlation not just with intelligence, but with a reduction in risk of unrelated conditions.

That included Alzheimer’s and ADHD. It also found an association with higher indications of intelligence and both longer lives and greater incidence of autism.

The two new studies rely on the increasingly large number of people who have been genotyped, a form of genetic analysis that identifies genetic traits rather than full gene sequences. Globally, hundreds of thousands of people have agreed to have their genetic data used anonymously in studies paired with a variety of health information, questionnaires, and cognitive tests. However, these studies rely almost entirely on people living in the United States and a few European countries.

A meta-analysis relies on re-examining data from multiple studies with enough of a basis of similarity to remove error and reinforce key findings via statistical methods. As a result, meta-analyses can sometimes throw findings of a group of studies into doubt, or provide even more rigorous reinforcement.

These two studies, rather than providing firm conclusions, offer enormous guidance for further research that more directly connects and tests the statistical analyses.

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