Hoyer S
Institut for Patochemie und Allgemeine Neurochemie, Ruprecht-Karis Universitat, Heidelberg, Germany.
Acta Neurol Scand Suppl. 1996;165:18-24. doi: 10.1111/j.1600-0404.1996.tb05868.x.
Glucose metabolism in the brain has an important influence on many normal cellular processes. It contributes to the synthesis of acetylcholine, glutamate, aspartate, gamma-aminobutyric acid, glycine, and ATP production (the driving force behind almost all cellular and molecular activity). Neuronal glucose metabolism is controlled antagonistically by insulin and cortisol. Desensitization of the neuronal insulin receptor causes abnormalities in oxidative energy metabolism. During normal aging, the cerebral energy pool is slightly diminished, but its level increases after stressful events. In age-related sporadic late-onset dementia of the Alzheimer type (SDAT), glucose metabolism and formation of cellular energy are severely reduced. Desensitization of the neuronal insulin receptor seems to be an early event in the pathogenesis or even etiology of SDAT causing disturbances in oxidative glucose metabolism and energy failure in insulin-sensitive brain structures. These abnormalities appear to induce a cascade of disturbances that leads to abnormal APP processing and amyloid formation, membrane damage, and neuronal death.
大脑中的葡萄糖代谢对许多正常细胞过程具有重要影响。它有助于乙酰胆碱、谷氨酸、天冬氨酸、γ-氨基丁酸、甘氨酸的合成以及ATP的产生（几乎所有细胞和分子活动背后的驱动力）。神经元葡萄糖代谢受胰岛素和皮质醇的拮抗控制。神经元胰岛素受体的脱敏会导致氧化能量代谢异常。在正常衰老过程中，大脑能量储备会略有减少，但在应激事件后其水平会升高。在与年龄相关的散发性晚发性阿尔茨海默型痴呆（SDAT）中，葡萄糖代谢和细胞能量形成会严重减少。神经元胰岛素受体的脱敏似乎是SDAT发病机制甚至病因中的早期事件，会导致胰岛素敏感脑结构中的氧化葡萄糖代谢紊乱和能量衰竭。这些异常似乎会引发一系列紊乱，导致异常的APP加工和淀粉样蛋白形成、膜损伤以及神经元死亡。
