您大脑智力衰退快吗?科学家找到影响大脑年龄基因
How Fast Will Your Brain Age? Scientists Identify Key Gene
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2019-12-06 06:27
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火星译客

Your brain may start aging at a dramatically faster rate when you hit age 65 — or it may not, depending on which version of a particular gene you have, a new study suggests.

年龄刚到65岁,有的人大脑以戏剧性速度开始衰退,有的不会。科学家最近新研究发现,这完全取决于一种特殊遗传基因形式。

In the study, scientists identified a gene that appears to control the speed at which the brain ages, and they say that a particular version of it may offer protection against a host of age-related neurological diseases, including dementia. [7 Ways the Mind and Body Change With Age]

科学家发现了一种能控制大脑衰老速度的一种基因。科学家认为,这种基因特殊变异形式能防止随老人年龄增大而引起的神经性疾病,其中包括老年痴呆症。[衰老引起的智力和躯体器官7种变化 ]

The gene, called TMEM106B, kicks into action at about age 65. Soon after that, people with bad copies of this gene will have a brain that looks 10 to 12 years older than people of the same age who have working copies, the scientists said.

这种被称作TMEM106B基因大概在65岁左右年龄中的老人发挥作用。65岁之后,大脑有劣质基因拷贝的老人比正常基因拷贝的同龄人苍老10岁到12岁。

The discovery may allow doctors to identify which people are at an increased risk for neurological diseases by virtue of having a faulty TMEM106B gene. It also may help develop drugs that target this gene to promote healthier brain aging, the researchers said. The study describing this work appears today (March 15) in the journal Cell Systems.

研究人员指出,这个发现有助于医生通过缺陷TMEM106B基因变异,确认病人是否存在神经系统疾病风险,有助于药品厂家靶向该基因开发新药,有利于人类大脑健康。该项研究论文于今天(3月15日)发表在《细胞系统(Cell Systems)》杂志上。

In recent years, scientists have identified numerous genes associated with Alzheimer's disease, Parkinson's disease and other neurological conditions.

最近几年,科学家们对阿尔茨海默症、帕金森病(Alzheimer's disease, Parkinson's disease)和其它神经系统疾病进行了大量研究并找出了各种致病基因。

"But those genes explain only a small part of these diseases," said study co-leader Herve Rhinn, an assistant professor of pathology and cell biology in the Taub Institute for Alzheimer's Disease and the Aging Brain at Columbia University Medical Center in New York. "By far, the major risk factor for neurodegenerative disease is aging. Something changes in the brain as you age that makes you more susceptible to brain disease."

“但是,这些基因仅是致病原因很小部分”该项研究合作者、位于纽约的哥伦比亚大学医学中心陶布研究所(Taub Institute)的病理学与细胞生物学助理教授荷芙·莱恩(Herve Rhinn)说,“迄今为止,神经退行性疾病(neurodegenerative disease)是衰老主要危险因素。年龄大了之后,大脑发生变化更易诱发大脑疾病。” 莱恩一直在从事阿尔茨海默症疾病和大脑衰老研究。

The genetic-based instructions expressed by TMEM106B may be that "something," Rhinn said. The instructions may either protect against or accelerate the ravages of aging. [6 Big Mysteries of Alzheimer's Disease]

莱恩认为,这种“变化”或许就是TMEM106B基因变异表达的指令,这种指令能延缓衰老也能加速衰老。 [阿尔茨海默症疾病的6大谜团(6 Big Mysteries of Alzheimer's Disease)]

"If you look at a group of seniors, some will look older than their peers, and some will look younger," said Dr. Asa Abeliovich, a professor of pathology and neurology at the Taub Institute and a co-author of the study. "The same differences in aging can be seen in the frontal cortex, the brain region responsible for higher mental processes."

“不妨去看看一群长者,有些比同龄人老,有些比同龄人年轻,”该课题研究人员之一、陶布研究院所病理学和神经病学教授亚撒·亚伯里奥维契(Asa Abeliovich)博士说,“衰老差异在大脑前额皮层同样存在,前额皮层是大脑高级认知区域。”

Previous studies have associated TMEM106B with a rare form of dementia called frontotemporal lobar degeneration. However, the new study shows that the TMEM106B gene is more broadly associated with brain age, and underlies how well seniors maintain their cognitive abilities, according to Rhinn and Abeliovich.

莱恩和亚伯里奥维契指出,早期对TMEM106B的研究只是涉及额颞叶变性痴呆症少数病例。现在发现,TMEM106B基因变异与大脑衰老密切相关,它是长者保持良好认知能力的基础。

To determine what might control brain aging, the two researchers analyzed genetic data from more than 1,200 autopsied human brains from people who had not been diagnosed with a neurodegenerative disease while alive. They focused on a few hundred genes whose levels of expression had previously been found to either increase or decrease with aging. From this information, they compiled a chart of what they called "differential aging" denoting the difference between someone's true or chronological brain age compared with an apparent brain age.

为寻找控制大脑衰老方法,二位研究人员分析了1,200多名死者尸体解剖的大脑基因数据。这些人活着的时候并没有诊断出神经退行性疾病。研究人员着重对已经发现的影响大脑衰老(加速与减缓)的上百个基因进行研究。根据这些资料,他们绘制一种图表,称作“差异衰老”图,显示真实或实足大脑年龄(true or chronological brain age)与外观大脑年龄的差异。

One gene, TMEM106B, popped out of the data as a genetic driver of differential aging. TMEM106B appears to control inflammation and neuronal loss in the brain. There are two forms of the gene, or alleles: One form is associated with an increased rate, or risk, of brain aging, and the other allele is protective and is thought to prevent such an acceleration of aging.

TMEM106B基因变异数据具有大脑衰老驱动器作用,似乎能控制大脑炎症和神经元失调。它的变异形式(等位基因)有二种:一种增加大脑衰老速率(风险);另一种延缓大脑衰退,即防止大脑加速老化。

Everyone has two copies of the gene, and in the general population, about 30 percent of people have two risk alleles; about 50 have one risk allele and one protective allele; and 20 percent have two protective alleles, Rhinn said. [6 Foods That Are Good For Your Brain]

莱恩认为,每个人的基因都有二种拷贝。一般来说,大约30%的人有二个风险等位基因;大约50%有一个风险等位基因和一个保护等位基因;大约20%的人有二个保护等位基因。 [ 6种健脑食品 ]

"From what we could see, the effect of the [TMEM106B] risk allele is additive, in the sense that the brain of elderly people with two copies of the risk allele 'looks' five years older than the [brain] of people with only one copy of risk allele, and [they] themselves 'look' five years older than people with no risk allele," Rhinn told Live Science. "It is indeed one of our hypotheses that TMEM106B regulates systematic response to age-associated stressors in [the] human brain."

“我们发现,TMEM106B风险等位基因的作用是累积的,在某种意义上说,有二个风险等位基因拷贝的老人大脑(brain of elderly people)比一个风险等位基因拷贝的老人老五岁,而后者又比没有风险等位基因拷贝老人外貌老五岁。” 莱恩告诉生活科学(Live Science)说,“我们设想,TMEM106B对人类大脑年龄压力系统的应答确有调节作用。”

In the same study, Rhinn and Abeliovich also looked at the brains of people who had been affected by Alzheimer's disease and/or Huntington's disease during their lives, and they observed the same effect of TMEM106B on brain aging in those people.

在该项研究中,莱恩和亚伯里奥维契还研究了阿茨海默症和亨廷顿氏症疾病患者生前大脑。研究发现,这些人群中大脑衰老同样受到TMEM106B作用影响。

"TMEM106B begins to exert its effect once people reach age 65," Abeliovich said. "Until then, everybody's in the same boat, and then there's some yet-to-be-defined stress that kicks in. If you have two good copies of the gene, you respond well to that stress. If you have two bad copies, your brain ages quickly."

“老人进入65岁年龄后,TMEM106B就发挥作用”。亚伯里奥维契说,“到那时,所有人都有在同一条船上,承受压力各有不同。如果基因拷贝二个都健康,就能很好应对这种压力(respond well to that stress.)。若有二个拷贝都低劣,大脑就会迅速才老化。”

TMEM106B may be an attractive target for researchers hoping to create treatments that could slow down brain aging, although such therapies would take many years to develop, the researchers said.

许多科研人员说,为减缓大脑衰老速度,他们对TMEM106B怀有巨大兴趣,希望能开发一种新的防治大脑衰退医疗方法,尽管这个过程要经历若干年。

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