题型：阅读理解 题类：常考题 难易度：普通
江苏省高邮市2018-2019学年度高一下学期英语期中调研试卷（音频暂未更新）
Depression(抑郁) can be a destructive illness, plaguing millions of people worldwide with feelings of sadness, hopelessness, and fatigue. Despite numerous antidepressant drugs, as many as a third of patients don't respond to medication. This has forced doctors to be more creative in finding different treatments for the condition.
In the past two decades, researchers have tied depression to a seemingly unrelated condition: inflammation(炎症), the body's natural response to stress. It could rise from injury or inflection, or even emotional issues like an unhappy marriage or problems at work. Some amount of inflammation is generally beneficial, as it increases production of cytokines(致癌因子)，proteins that help us heal and protect us from the effects of overwork.
But excessive cytokine levels, and the inflammation they bring on, could come at a cost—a number of studies suggests that high levels of cytokines could contribute to depression.
Cytokines can reach the brain several ways: directly through the blood-brain barrier or indirectly by binding to nerve fibers elsewhere, which send signals to the brain to produce the inflammation molecules. In the brain, cytokines can disturb the production and release of several important signaling chemicals, including serotonin, dopamine and glutamate, which help control emotion, appetite, sleep, learning and memory. It's though that a lack of serotonin activity in the brain causes depression; most antidepressants increase the activity. But cytokines also have been shown to activate stress hormone signaling in the brain, which man also serve to develop depression.
With all the evidence implicating inflammation in depression, doctors have been anxious to test anti-inflammatory drugs as a potential treatment. Four small studies published between 2006 and 2017 by research groups in Europe and Iran found that adults diagnosed with depression who took aspirin or another anti-inflammatory drug called Celecoxib, along with an antidepressant, got more relief from feelings of sadness, hopelessness, guilt and fatigue compared with those taking an antidepressant alone. However, Andrew Miller, a professor of psychiatry at Emory University, thought something was wrong in these small, limited studies. None of them looked at whether the participants had to have high levels of cytokines before they'd see a benefit from anti-inflammatory drugs. "Unfortunately, much of the field has fallen into the trap of viewing inflammation as the be-all, end-all," Miller says. He and his colleagues wanted to see whether the effect of these drugs was limited to the depression patients with high cytokine levels, or if it helped all people diagnosed with depression.
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