过剩3
过剩1
糖酵解
内科学
葡萄糖转运蛋白
内分泌学
发病机制
碳水化合物代谢
葡萄糖稳态
平衡
葡萄糖摄取
丝氨酸
医学
焊剂(冶金)
生物
新陈代谢
化学
生物化学
糖尿病
胰岛素抵抗
胰岛素
有机化学
酶
作者
Yang An,Vijay R. Varma,Sudhir Varma,Ramon Casanova,Eric B. Dammer,Olga Pletniková,Chee W. Chia,Josephine M. Egan,Luigi Ferrucci,Juan C. Troncoso,Aĺlan I. Levey,James J. Lah,Nicholas T. Seyfried,Cristina Legido‐Quigley,Richard O’Brien,Madhav Thambisetty
标识
DOI:10.1016/j.jalz.2017.09.011
摘要
Abstract Introduction It is unclear whether abnormalities in brain glucose homeostasis are associated with Alzheimer's disease (AD) pathogenesis. Methods Within the autopsy cohort of the Baltimore Longitudinal Study of Aging, we measured brain glucose concentration and assessed the ratios of the glycolytic amino acids, serine, glycine, and alanine to glucose. We also quantified protein levels of the neuronal (GLUT3) and astrocytic (GLUT1) glucose transporters. Finally, we assessed the relationships between plasma glucose measured before death and brain tissue glucose. Results Higher brain tissue glucose concentration, reduced glycolytic flux, and lower GLUT3 are related to severity of AD pathology and the expression of AD symptoms. Longitudinal increases in fasting plasma glucose levels are associated with higher brain tissue glucose concentrations. Discussion Impaired glucose metabolism due to reduced glycolytic flux may be intrinsic to AD pathogenesis. Abnormalities in brain glucose homeostasis may begin several years before the onset of clinical symptoms.
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