新研究显示，神经元缺失是老年失眠元凶 [复制链接]

It's long been known that the older you get, the less you sleep. There are many proposed reasons for why this happens, and they include new medications, psychological distress, retirement or simply the theory that the elderly need less sleep.


But a new study from Beth Israel Deaconess Medical Center and University of Toronto researchers offers, for the first time, a neurological reason for the phenomenon: namely, that a specific cluster of neurons associated with regulating sleep patterns, called the ventrolateral preoptic nucleus, may slowly die off as you get older.


"The more of these cells you lose from aging, the harder time you have sleeping," lead researcher Clifford Saper, M.D., Ph.D., chairman of neurology at the Beth Israel Deaconess Medical Center, told HuffPost.


Saper noted that by the time people are in their 70s, they’re generally sleeping an hour and a half less than they did when they were in their 20s. "They’re not feeling rested -- they're getting up because they can't sleep anymore, but they're still tired during the day," he said. "It’s sort of a chronic insomnia state."


The new findings, published in thejournal Brain, could one day lead to development of medication that would smooth disrupted sleep patterns by specifically targeting the neurons pinpointed in the study -- and it would do so without negatively affecting other functions, like balance, the way some current sleep medications do, explained Saper.


Saper first linked the death of the neurons to sleep disruption in studies with lab rats, finding that the animals who didn't have them suffered "profound insomnia."


He then sought to replicate his findings in human subjects. Saper analyzed a dataset of almost 1,000 subjects who had entered into a memory and aging study back in 1997, when they were all healthy 65-year-olds. As part of the study, they had all agreed to wear a small watch-sized device on their wrists for about 7 to 10 days, every two years, that would record all their movements. Upon their deaths, their brains were donated to science, so research could continue.


Saper chose 45 brains to examine, based on whether or not the ventrolateral preoptic nucleus was still intact. First he stained the brain in order to find the cluster of neurons, which were located in a similar part of the human brain as the rats' brains.


Then he linked the neurons found in the brain to the rest-activity behavior data collected in that person's final year of life. He found that the fewer neurons one had, the more sleep fragmentation that person experienced in the last year of life. Brains with the largest amount of neurons (over 6,000) belonged to people with longer, uninterrupted sleep.


Another key finding from the study: The link between fewer neurons and less sleep was even more pronounced in people who had died with Alzheimer's disease.


"The surprise finding was that people with Alzheimer's disease lose these cells particularly quickly," said Saper. "Those were the ones with the very fewest neurons and the most disrupted sleep."


Because people with Alzheimer's disease often end up being institutionalized over the issues that can stem from disrupted sleep (like nighttime wandering), Saper said his Alzheimer's finding may be "key" to figuring out how to keep those patients home with family members.


"If we could develop medications that helped Alzheimer's patients sleep through the night, without causing them to have increased risk of falling, this could keep some people out of nursing homes," he said.


Anna Almendrala annaa@huffingtonpost.com



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It's long been known that the older you get, the less you sleep. There are many proposed reasons for why this happens, and they include new medications, psychological distress, retirement or simply the theory that the elderly need less sleep.
众所周知随着年龄增加,睡眠也随之减少. 对此导致的原因社会上有很多解释例如新药, 心理困扰, 退休,甚至简单的解释为老年人只需要少量的睡眠.

But a new study from Beth Israel Deaconess Medical Center and University of Toronto researchers offers, for the first time, a neurological reason for the phenomenon: namely, that a specific cluster of neurons associated with regulating sleep patterns, called the ventrolateral preoptic nucleus, may slowly die off as you get older.
但是根据贝斯以色列女执事医疗中心和多伦多大学的研究员提出了新的研究, 也是首次提出由于神经原因导致人类随着年龄增加所需睡眠减少的解释, 即神经元簇(腹前核)可以调控睡眠模式会随着年龄的增加缓慢的减少。

"The more of these cells you lose from aging, the harder time you have sleeping," lead researcher Clifford Saper, M.D., Ph.D., chairman of neurology at the Beth Israel Deaconess Medical Center, told HuffPost.
“ 随着年龄增加这些神经元细胞失去的越多，你越难以入睡”，贝斯以色列女执事医疗中心的首席研究员 医学博士，神经学主席克利福德 塞波告诉哈夫波斯特。



Saper noted that by the time people are in their 70s, they’re generally sleeping an hour and a half less than they did when they were in their 20s. "They’re not feeling rested -- they're getting up because they can't sleep anymore, but they're still tired during the day," he said. "It’s sort of a chronic insomnia state."
塞波博士强调通常人们到70几岁时睡眠时间要比他们20几岁时少1个半小时。塞波博士说他们早醒之后无法再入睡无法躺在床上休息只能提早起床，精神不充沛他们白天仍然会觉得疲倦。是种慢性失眠症。


The new findings, published in thejournal Brain, could one day lead to development of medication that would smooth disrupted sleep patterns by specifically targeting the neurons pinpointed in the study -- and it would do so without negatively affecting other functions, like balance, the way some current sleep medications do, explained Saper.
  新的发现发布在《脑》杂志，塞波博士解释在精确定位神经元的研究中，未来有望开发一种药可以温和的中断睡眠模式。不会像现在市面上的治疗失眠的药物一，这种新药不会对其他身体功能造成负面的影响。

Saper first linked the death of the neurons to sleep disruption in studies with lab rats, finding that the animals who didn't have them suffered "profound insomnia."
塞波博士开始时在实验鼠上研究睡眠中断与神经元死亡关联，他发现这些动物不会受严重的失眠困扰。



He then sought to replicate his findings in human subjects. Saper analyzed a dataset of almost 1,000 subjects who had entered into a memory and aging study back in 1997, when they were all healthy 65-year-olds. As part of the study, they had all agreed to wear a small watch-sized device on their wrists for about 7 to 10 days, every two years, that would record all their movements. Upon their deaths, their brains were donated to science, so research could continue.
然后，他企图在人的身上也能有同样的发现。 塞波博士分析 早在1997年开始了约有1000位身体健康的65岁老年人作为志愿者参与的关于年龄和记忆的研究数据。 作为研究的组成部分，这些人员全部同意在每两年7到10天在手腕上佩戴手表大小的装置，可以记录他们的日常活动。即使他们去世，为了研究可以继续， 他们的大脑仍然供于科学研究。

Saper chose 45 brains to examine, based on whether or not the ventrolateral preoptic nucleus was still intact. First he stained the brain in order to find the cluster of neurons, which were located in a similar part of the human brain as the rats' brains.
塞波博士选择了45 个脑检查腹前核是否完好。 首先他为了发现神经簇将大脑染色，鼠脑相似的位置在人脑中发现神经簇。

谢谢梦舒的翻译。

Then he linked the neurons found in the brain to the rest-activity behavior data collected in that person's final year of life. He found that the fewer neurons one had, the more sleep fragmentation that person experienced in the last year of life. Brains with the largest amount of neurons (over 6,000) belonged to people with longer, uninterrupted sleep.
然后他把大脑中发现的神经元与收集的志愿者的晚年生活的静息活动行为数据联系一起分析。 他发现一个人的神经元越少，在他们晚年睡眠碎片越多。 脑中巨量（超过6000）这样的神经元可以使人保有长时间，无中断的睡眠。

Another key finding from the study: The link between fewer neurons and less sleep was even more pronounced in people who had died with Alzheimer's disease.
在研究中另一重要发现，神经元越少，睡眠也随之减少 可能是导致人患阿尔茨海默病死亡的原因

"The surprise finding was that people with Alzheimer's disease lose these cells particularly quickly," said Saper. "Those were the ones with the very fewest neurons and the most disrupted sleep."
塞波博士说：“ 惊讶的发现患有阿尔茨海默病的人神经元减少的特别快。他们具有非常少的神经元及睡眠质量极其不好.


Because people with Alzheimer's disease often end up being institutionalized over the issues that can stem from disrupted sleep (like nighttime wandering), Saper said his Alzheimer's finding may be "key" to figuring out how to keep those patients home with family members.
因为患有阿尔茨海默病的人由于 睡眠中断( 例如 夜游 )而导致其生命危险, 塞波博士说他的发现可能其关键作用使患阿尔茨海默病的人与家人在一起生活
"If we could develop medications that helped Alzheimer's patients sleep through the night, without causing them to have increased risk of falling, this could keep some people out of nursing homes," he said.
如果我们能研发出新药可以帮助晚上阿尔茨海默病人睡觉时避免出现意外的危险, 也能使一些患阿尔茨海默病人无需住养老院.

阿尔茨海默病（AD）是一种起病隐匿的进行性发展的神经系统退行性疾病。临床上以记忆障碍、失语、失用、失认、视空间技能损害、执行功能障碍以及人格和行为改变等全面性痴呆表现为特征，病因迄今未明。65岁以前发病者，称早老性痴呆；65岁以后发病者称老年性痴呆。

The ventrolateral preoptic nucleus (VLPO) is a small cluster of neurons situated in the anterior hypothalamus, to the side of the optic chiasm in the mammalian brain. The VLPO is active during sleep, primarily during non-rapid eye movement sleep (NREM sleep), and releases inhibitory neurotransmitters, mainly GABA and galanin, which inhibit neurons that are involved in wakefulness and arousal.
腹前核( VLPO) 是以小簇神经元位于下丘脑前叶, 哺乳动物大脑视交叉神经边上. 在睡觉期间, VLP。O 是活动状态， 基本上是非快速眼球运动睡眠和释放抑制神经传递（γ-氨基丁酸和甘丙肽）抑制神经元使人觉醒  

γ-氨基丁酸（简称GABA）是一种天然存在的非蛋白质氨基酸，是哺乳动物中枢神经系统中重要的抑制性神经传达物质，约30%的中枢神经突触部位以GABA为递质。在人体大脑皮质、海马、丘脑、基底神经节和小脑中起重要作用，并对机体的多种功能具有调节作用。当人体内GABA缺乏时，会产生焦虑、不安、疲倦、忧虑等情绪，一般长久处于高压力族群如身处竞争环境中的人群、运动员、上班族等，都很容易缺乏GABA需要及时补充以便舒缓情绪。

Galanin(甘丙肽)是一种在中枢神经系统中广泛分布的神经肽,功能涉及摄食、睡眠和觉醒、疼痛、认知和生殖等各方面

我睡眠很好，是不是意味着我的神经元退化很少啊？哈哈哈

睡眠是健康之源，健康之本，有了好的睡眠，才有好的健康。无论从心心理层面还是躯体层面来看，睡眠都是第一位的。


我们社会对此不够重视，大家说起养生，都会说体育锻炼，吃营养食物。其实，最重要的是修炼睡眠能力，睡眠需要静心，对人间烦恼学会放下，睡眠可以激活免疫细胞等等。


那么怎样才能修炼睡眠呐？首先，累了就去睡，不要轻意挑战睡眠阈值。睡眠能力可以培养的，尽早培养尽早得意。等老年人了，再修炼会增加难度。第二，积极心理暗示自己。偶尔一次睡眠不好，就给自己扣帽子，说，我睡眠不好，心理的东西，不可以消极暗示，会起作用。自己身体休息系统会调节的，当偶尔一次睡眠不好的时候，不要担心。过些时候，神经兴奋期过了，她会疲劳的，会自动补睡的。你只要流出时间空间给她，就可以了。第三，重视睡眠，记得，比吃药打针还有效，可以不吃，不聊天，不看视频，但是一定要首先睡眠。第四，做一点简单劳动或运动，让自己体力疲劳，然后睡觉。第五，最难的，也是很关键的一环，就是修心了，学会随意，放下烦恼。自然睡眠就好了。