Background

Depression is known to be a risk factor for Alzheimer's disease (AD). Changes in amyloid β protein (Aβ) metabolism have been speculated as a factor contributing to the transition from depression to AD. The aim of this study is to reveal the time course and state-dependency of Aβ metabolism.

Methods

Serum Aβ levels in 277 elderly (≥60 years) patients with depression (both early- and late-onset) were measured at admission, immediately after remission, and 1 year after remission, and compared them with 178 healthy subjects.

Results

The analysis revealed decreased Aβ42 levels and increased Aβ42/40 ratios in elderly patients with depression at admission compared with healthy subjects. These changes in the acute phase of depression were not normalized immediately after remission; however, they recovered to healthy levels 1 year after remission.

Limitations

There is a possibility that the results may be influenced by antidepressants.

Conclusions

These results suggest that altered Aβ metabolism caused by depression may ameliorate, although after a lengthy period of time after remission. Our findings also suggest that the AD-related pathological changes caused or increased by depression can be reduced by maintaining remission for an extended period of time.

中文翻译：

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老年抑郁症患者临床病程及血清β-淀粉样蛋白水平

背景

众所周知，抑郁症是阿尔茨海默病 (AD) 的危险因素。淀粉样蛋白 β 蛋白 (Aβ) 代谢的变化已被推测为促成从抑郁症向 AD 转变的一个因素。本研究的目的是揭示 Aβ 代谢的时间过程和状态依赖性。

方法

在入院时、缓解后立即和缓解后 1 年测量了 277 名老年（≥60 岁）抑郁症患者（早发和晚发）的血清 Aβ 水平，并将其与 178 名健康受试者进行比较。

结果

分析显示，与健康受试者相比，老年抑郁症患者入院时 Aβ42 水平降低，Aβ42/40 比值升高。抑郁症急性期的这些变化在缓解后并未立即恢复正常；然而，他们在缓解一年后恢复到健康水平。

限制

结果可能会受到抗抑郁药的影响。

结论

这些结果表明，抑郁症引起的 Aβ 代谢改变可能会改善，尽管在缓解后很长一段时间后。我们的研究结果还表明，抑郁症引起或增加的 AD 相关病理变化可以通过长时间维持缓解来减少。