Maeba Ryouta, Araki Atsushi, Ishii Kenji, Ogawa Kishiko, Tamura Yoshiaki, Yasunaga Masashi, Minami Ushio, Komori Aya, Okazaki Tomoki, Nishimukai Megumi, Hara Hiroshi, Fujiwara Yoshinori
Department of Biochemistry, Teikyo University School of Medicine, Tokyo, Japan.
Department of Diabetes, Metabolism and Endocrinology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan.
Clin Chim Acta. 2016 Jan 30;453:134-40. doi: 10.1016/j.cca.2015.12.007. Epub 2015 Dec 8.
Several reports have implicated myo-inositol (MI) in myelin formation. We hypothesized that MI is involved in this process through facilitating the biosynthesis of ethanolamine plasmalogens (PlsEtns), which are the major component of myelin membranes, and essential for myelin formation and function. Excessive MI urinary excretion possibly causes PlsEtn deficiency, leading to demyelinating diseases including dementia.
We examined the association between cognitive impairment, serum levels of PlsEtn, and baseline levels of urinary MI excretion, in the enrollment of 55 memory clinic outpatients and 107 cognitively normal elderly.
Serum PlsEtns were independently associated with cognitive impairment, and significantly reduced in memory clinic outpatients, especially in those with high urinary MI, as compared to normal elderly. On the other hand, there was no direct association between urinary MI and cognitive impairment, but urinary MI was significantly associated with serum hemoglobin A1c and amyloid β 1-40. The interaction between PlsEtn and urinary MI for cognitive impairment was statistically confirmed, and their combined usage improved diagnosis of cognitive impairment.
We proposed the involvement of MI and PlsEtn in cognitive impairment pathology. In conclusion, serum PlsEtn may be useful in detecting cognitive decline among elderly with hyperglycemia.
多项报告表明肌醇(MI)参与髓鞘形成。我们推测,MI通过促进乙醇胺缩醛磷脂(PlsEtns)的生物合成参与这一过程,PlsEtns是髓鞘膜的主要成分,对髓鞘形成和功能至关重要。MI尿排泄过多可能导致PlsEtn缺乏,进而引发包括痴呆症在内的脱髓鞘疾病。
我们在55名记忆门诊患者和107名认知正常的老年人中,研究了认知障碍、血清PlsEtn水平与尿MI排泄基线水平之间的关联。
血清PlsEtns与认知障碍独立相关,与正常老年人相比,记忆门诊患者血清PlsEtns显著降低,尤其是尿MI水平高的患者。另一方面,尿MI与认知障碍之间无直接关联,但尿MI与血清糖化血红蛋白A1c和淀粉样β蛋白1-40显著相关。经统计学证实,PlsEtn与尿MI在认知障碍方面存在相互作用,二者联合使用可改善认知障碍的诊断。
我们提出MI和PlsEtn参与认知障碍病理过程。总之,血清PlsEtn可能有助于检测高血糖老年人的认知衰退。