Inoue Megumi, Baba Hajime, Yamamoto Keiichi, Shimada Hiroyuki, Yamakawa Yoshihiro, Suzuki Toshihito, Miki Takami, Arai Heii
Juntendo University Mood Disorder Project, Department of Psychiatry, Juntendo Koshigaya Hospital, Saitama, Japan; Department of Psychiatry & Behavioral Science, Juntendo Graduate School of Medicine, Tokyo, Japan.
Juntendo University Mood Disorder Project, Department of Psychiatry, Juntendo Koshigaya Hospital, Saitama, Japan; Department of Psychiatry & Behavioral Science, Juntendo Graduate School of Medicine, Tokyo, Japan.
Am J Geriatr Psychiatry. 2016 Sep;24(9):764-72. doi: 10.1016/j.jagp.2016.05.005. Epub 2016 May 18.
Epidemiologic studies have demonstrated that suffering from depression may be a risk for Alzheimer disease (AD). As a possible biologic mechanism underlying the transition from depression to AD, it has been speculated that pathologic changes in β-amyloid (Aβ) metabolism are involved. To further understand the peripheral kinetics of amyloid in patients with depression, we investigated serum levels of free Aβ and albumin-bound Aβ.
Seventy inpatients with DSM-IV major depressive disorder (MDD) and 81 healthy individuals (the comparison group) were recruited between June 2012 and February 2014. Serum Aβ40 and Aβ42 levels, Aβ40/Aβ42 ratio, and serum levels of albumin-Aβ complexes (SLAACs) were compared between the comparison group and patients in two age groups comprising younger (<60 years) and elderly (≥60 years) people.
SLAAC was decreased in older patients with MDD but not in younger patients. The serum-free Aβ40/Aβ42 ratio was higher in patients with depression, even in younger patients.
Our findings suggest that free Aβ and the albumin-bound Aβ reflect a different serum amyloid kinetics in depression. We speculate that serum-free Aβ reflects changes in amyloid metabolism in patients suffering from depression and albumin-bound Aβ reflects AD pathology and may be a potential predictor of the prodromal stage of AD.
流行病学研究表明,患抑郁症可能是患阿尔茨海默病(AD)的一个风险因素。作为从抑郁症向AD转变的一种可能的生物学机制,有人推测β-淀粉样蛋白(Aβ)代谢的病理变化与之有关。为了进一步了解抑郁症患者外周淀粉样蛋白的动力学,我们研究了游离Aβ和与白蛋白结合的Aβ的血清水平。
在2012年6月至2014年2月期间招募了70例符合DSM-IV标准的重度抑郁症(MDD)住院患者和81名健康个体(对照组)。比较了对照组与年龄在60岁以下的年轻患者和60岁及以上的老年患者这两个年龄组患者的血清Aβ40和Aβ42水平、Aβ40/Aβ42比值以及白蛋白-Aβ复合物(SLAACs)的血清水平。
老年MDD患者的SLAAC降低,但年轻患者未降低。抑郁症患者,甚至是年轻患者,其血清游离Aβ40/Aβ42比值更高。
我们的研究结果表明,游离Aβ和与白蛋白结合的Aβ在抑郁症中反映了不同的血清淀粉样蛋白动力学。我们推测,血清游离Aβ反映了抑郁症患者淀粉样蛋白代谢的变化,而与白蛋白结合的Aβ反映了AD病理,可能是AD前驱期的一个潜在预测指标。