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抑郁症的生理机制、危害与治疗 – 译学馆
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抑郁症的生理机制、危害与治疗

Depression and its treatment

《自然视频》
Nature Video
《自然神经科学》
Nature Neuroscience
展示抑郁症及其治疗方法
present depression and its treatment
生活中 每个人都经历着
Mood naturally fluctuates and
情绪的时起时伏的自然波动
everyone experiences highs and lows in their lives.
但在某些情况下 情绪的变化会持续很长时间
But in some cases changes in mood can become long-lasting
使人变得虚弱并难以胜任工作
Debilitating and can impair someone’s ability to hold down a job,
或难以维持正常的人际关系
or sustain meaningful relationships
估计大约有10%的人
It’s estimated that around 10 percent of people will
在生命的某个阶段会患上抑郁症
will at some point in their lives suffer from depression.
这是一种情绪障碍 一些典型症状有
A mood disorder, characterized by several symptoms,
伤心 痛苦
feeling sad, distressed,
缺乏干劲 感到精疲力尽
unmotivated, excessively tired,
并对曾经热衷的活动失去兴趣 也即快感缺乏
and losing interest in once pleasurable activities known as anhedonia.
很多抑郁症患者也遭受焦虑的折磨
Many people with depression also suffer from anxiety.
神经影像学研究发现
Neuroimaging studies reveal
许多正常调节情绪的脑回路在抑郁症患者的大脑中是失调的
that many brain circuits that normally regulate mood are dysregulated in depression.
大脑深处的杏仁核
Located deep within the brain the amygdala
能快速处理刺激 比如奖励以及潜在的威胁
processes highly salient stimuli such as rewards and potential threats
抑郁时 杏仁核会异常活跃
In depression the amygdala is overactive
并对消极的事情反应过度
and responds excessively to negative events
杏仁核依次与一系列提升
In turn the amygdala connects to a set of brain regions
情绪刺激的生理和行为反应的大脑区域连接
that hone the physiological and behavioral response to emotional stimuli.
这些区域包括内侧前额叶皮质 伏核
These areas include the medial prefrontal cortex the nucleus accumbens
海马结构和脑岛
the hippocampus and the insula.
海马结构与记忆形成有关
The hippocampus is involved in memory formation and
和前额皮质一样极易受到压力的影响
along with the prefrontal cortex is particularly vulnerable to effects of stress
抑郁的人更容易受到压力的影响
Depressed people are more susceptible to stress
这会导致大脑的生理变化 包括海马结构萎缩
which can cause physical changes in the brain including atrophy of the hippocampus
抑郁症患者的这种变化和其他变化
This and other changes in depressed people
可能导致他们对情感事件有不适当的反应
may cause inappropriate responses to emotional events
内侧前额叶皮质参与调节
The medial prefrontal cortex is involved in regulating
我们对情感刺激的反应程度
how strongly we react to emotional stimuli.
如抗抑郁药 认知行为治疗 电击治疗等治疗方法
Treatments such as antidepressant drugs cognitive behavioral therapy and electroconvulsive therapy
会影响大脑各个区域的结构和功能
affect the structure and function of these and other brain regions
举一个动物模型的例子
Animal models such as mice
老鼠对于帮助我们理解抑郁症背后的细胞变化
are critical in helping us understand the cellular and molecular changes
和提出更好的治疗方法至关重要
underlying depression and develop better treatments.
虽然我们不可能知道一只老鼠是否抑郁
Although it’s impossible to know if a mouse is depressed.
但研究显示老鼠在慢性压力下
My subject to chronic stress
有些症状与抑郁患者的症状很像
shows some symptoms similar to depressed humans.
比如 焦虑 更少的社交互动
Such as anxiety like behavior less social interaction
以及对一般令人愉快的活动丧失兴趣
and a lack of interest in normally pleasurable activities.
尽管不是所有人的抑郁都由压力引起
While not all human depression is triggered by stress.
这些模型仍可能有助于阐明抑郁症的生物学原理
These models may still shed light on the biology of depression
这是科学家在研究老鼠时得到的最密切的数据
and they’re the closest scientists can get while studying mice.
和人类一样 慢性压力同样能导致老鼠的
As with humans, chronic stress in mice can lead to
海马结构和前额皮质的萎缩
atrophy of the hippocampus and prefrontal cortex
对老鼠的研究 也显示出大脑的不同区域
Mouse studies have also shown altered neuronal plasticity
包括海马结构
in various brain regions including the hippocampus,
前额皮质 杏仁核和伏核中都出现了神经可塑性的变化
prefrontal cortex, amygdala, and nucleus accumbens.
在健康的海马结构中
In a healthy hippocampus,
经历可导致神经元之间连接的变化 表现为学习
experiences can lead to changes in the connections between neurons resulting in learning.
这种变化被称为可塑性
These changes are referred to as plasticity.
而慢性压力会降低这种可塑性
Chronic stress can reduce this plasticity
健康的大脑也会继续在海马结构的某个区域
Healthy brains also continue to produce new neurons
产生新的神经元
in one part of the hippocampus
这些新的神经元慢慢成熟
These new neurons slowly mature and integrate into the circuitry
并融入会对海马的活动和行为有很大影响的回路
where they have a strong effect on hippocampal activity and behavior
这些新的神经元也受压力的影响
These new neurons are also affected by stress.
在大脑紧张时 它们的数量不断减少
They reduced in number in stressed brains
这些影响可能是由于神经营养素水平的降低
These effects may result from reduced levels of neurotrophins,
而其是一种蛋白质 可以增加神经元的生长及可塑性
proteins that increase neuronal growth and plasticity.
可塑性的降低可能会使海马结构
Reduced plasticity may stop the hippocampus
无法正常调节压力反应
from being able to properly regulate the stress response
这可能会导致恶性循环
Which may lead to a vicious cycle
即压力会持续产生更多压力
where stress perpetuates more stress.
海马结构由此受到的影响尤甚
The hippocampus is particularly affected
除此之外 大脑其他区域也会出现可塑性的降低
But there can be reductions in plasticity elsewhere in the brain,
与此同时 这些变化
and together, these changes
会加重抑郁症的其他症状 如兴趣缺失
could contribute to other symptoms of depression like anhedonia.
不过在老鼠身上看到的这些细胞的变化
Whether these cellular changes seen in mice
是否与人类抑郁有关仍未可知
are involved in human depression remains unclear.
如今的大多数抗抑郁药物
Most antidepressants available today,
能迅速增加神经递质五羟色胺的数量
rapidly increase the amount of the neurotransmitters serotonin
和/或 突触里的去甲肾上腺素含量
and/or norepinephrine in the synapse.
然而病人和老鼠症状的好转
However improvements in symptoms in patients and mice
通常在治疗开始几周后才会出现
usually don’t occur until weeks after starting the treatment.
这种延迟的原因并不是非常清楚
While the reasons for this delay aren’t fully understood
长期使用抗抑郁药可以随着时间的推移
Prolonged treatment with antidepressants can over time act to
逆转由慢性压力引起的变化
reverse some of the changes induced by chronic stress,
增加神经营养因子表达并重建海马结构的可塑性
increasing neurotrophins expression and rebooting hippocampal plasticity.
对抑郁症的非化学治疗 包括电休克
Non-chemical treatments for depression including electroconvulsive shock
也可以促进老鼠的海马结构的可塑性
also promote hippocampal plasticity in mice.
抗抑郁治疗也可以逆转大脑其他区域
Antidepressant treatment can also reverse stress induced changes
因压力引起的变化
in other areas of the brain,
包括前额皮质和反馈回路区域产生的变化
including the prefrontal cortex and reward circuitry.
不同的治疗会针对不同的区域来改善症状
Different treatments may target different regions to improve symptoms
最近发现一种药品氯胺酮 对抑郁症患者有快速的抗抑郁作用
Recently the drug ketamine was found to have rapid antidepressant effects in patients with depression
对啮齿动物模型也有持续数日的效果
as well as in rodent models with effects lasting for days.
这背后的机制是一个活跃的研究领域
The mechanism behind this is an area of active research.
氯胺酮阻断一种突触传递
Ketamine blocks a type of synaptic transmission,
进而导致许多信号通路的激活
leading to activation of a number of signaling pathways,
以及神经营养因子表达的增加
and increasing neurotrophins expression.
这些分子的变化导致
These molecular changes result in increased plasticity
前额皮质和海马结构的可塑性增强
in the prefrontal cortex and hippocampus,
并且可能促进氯胺酮的行为效应
and likely contribute to ketamine’s behavioural effects.
通过研究由慢性压力造成的大脑的变化
By studying the changes in the brain caused by chronic stress
及像氯胺酮这样的抗抑郁药物是如何逆转这些变化的
And how antidepressants like ketamine work to reverse them?
研究人员可能会发现
Researchers may find new targets for treatment
比现有的治疗方法更快
or new drugs that could act more quickly,
更具体 或更有效的新的治疗目标或新药
more specifically or more effectively than currently available treatments.

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视频概述

主要介绍抑郁症的生理机制、产生后的危害以及抑郁症不同的治疗方法

听录译者

收集自网络

翻译译者

果松松

审核员

审核员 V

视频来源

https://www.youtube.com/watch?v=Yy8e4sw70ow

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