Waragai Masaaki, Adame Anthony, Trinh Ivy, Sekiyama Kazunari, Takamatsu Yoshiki, Une Kaori, Masliah Eliezer, Hashimoto Makoto
Department of Neurology, Higashi Matsudo Municipal Hospital, Matsudo-shi, Chiba, Japan.
Tokyo Metropolitan Institute of Medical Sciences, Setagaya-ku, Tokyo, Japan.
J Alzheimers Dis. 2016 Apr 8;52(4):1453-9. doi: 10.3233/JAD-151116.
Adiponectin (APN) is protective in animal models of neurodegenerative diseases, but the role of APN in human brain has not been established. Using an enzyme-linked immunosorbent assay, we found that APN was significantly decreased in cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD), compared to those in patients with mild cognitive impairment (MCI) and in normal controls (NC), despite elevation of APN in serum of patients with MCI and AD compared to that in NC. The discrepancy of CSF APN from serum APN in AD may suggest some critical actions of APN in the pathogenesis of AD. Indeed, it was histologically observed that APN was co-localized with tau in neurofibrillary tangles and immunoblot analysis showed that the functional trimers of APN were significantly decreased in AD compared to those in NC. Collectively, a loss of function of APN may be involved in the pathogenesis of AD.
脂联素（APN）在神经退行性疾病动物模型中具有保护作用，但APN在人脑中的作用尚未明确。通过酶联免疫吸附测定法，我们发现，与轻度认知障碍（MCI）患者及正常对照（NC）相比，阿尔茨海默病（AD）患者脑脊液（CSF）中的APN显著降低，尽管MCI和AD患者血清中的APN相较于NC有所升高。AD患者脑脊液APN与血清APN的差异可能提示APN在AD发病机制中具有某些关键作用。实际上，组织学观察发现APN与神经原纤维缠结中的tau蛋白共定位，免疫印迹分析表明，与NC相比，AD患者中APN的功能性三聚体显著减少。总体而言，APN功能丧失可能参与了AD的发病机制。
