It is well known that patients with Alzheimer's disease (AD) have imbalances in blood thiamine concentrations and lower activity of thiamine-dependent enzymes. Benfotiamine, a more bioavailable thiamine analog, has been proposed as an alternative to counteract these changes related to thiamine metabolism. Thus, our study aimed to analyze the effects of benfotiamine supplementation on brain thiamine absorption, as well as on parameters related to neuronal energy metabolism and disease progression in an experimental model of sporadic AD induced by intracerebroventricular injection of streptozotocin (STZ) in rats. The supplementation with 150 mg/kg of benfotiamine for 30 days increased the concentrations of thiamine diphosphate in the hippocampus and entorhinal cortex. This led to an improvement in mitochondria enzymes and insulin signaling pathway, with inactivation of GSK3α/β and ERK1/2, which are two tau-kinases related to the progression of AD, which could decrease tau hyperphosphorylation and apoptosis signaling. Besides, we observed an increased amount of Glun2b subunit of NMDA receptors, decreased inflammation, and improvement of cognitive deficit. Together, these results suggest that benfotiamine could be a potential therapeutic approach in the treatment of sporadic AD.

众所周知，患有阿尔茨海默氏病（AD）的患者血液中硫胺素浓度不平衡，硫胺素依赖性酶的活性较低。已经提出了一种可生物利用度更高的硫胺素类似物苯替丁胺，以抵消与硫胺素代谢有关的这些变化。因此，我们的研究旨在在大鼠脑室内注射链脲佐菌素（STZ）引起的散发性AD实验模型中，分析补充苯丁胺对脑硫胺素吸收的影响以及与神经元能量代谢和疾病进展相关的参数的影响。每天补充150 mg / kg的苯丁胺，持续30天，可增加海马和内嗅皮层中硫胺素二磷酸的浓度。这导致线粒体酶和胰岛素信号传导途径的改善，其中GSK3α/β和ERK1 / 2失活，这是与AD进展相关的两种tau激酶，可减少tau的过度磷酸化和细胞凋亡信号传导。此外，我们观察到NMDA受体的Glun2b亚基数量增加，炎症减少，认知障碍改善。在一起，这些结果表明，苯乙胺明可能是治疗散发性AD的潜在治疗方法。