领导这一研究的是复旦大学附属中山医院神经内科钟春玖教授和中科院神经科学研究所徐天乐研究员，前者早年毕业于安徽医科大学，主要研究方向为神经系统变性**、特别是老年性痴呆与帕金森病的发病机制与神经生化、神经干细胞应用，主要研究课题获卫生部青年科技基金、上海市科技基金(重点项目)等资助，先后在AmericanJournal of Neuroradiology（美国神经放射学杂志）等国内外权威与核心学术期刊发表论文30余篇。
老年痴呆症，又称阿尔茨海默病 (Alzheimer's disease,AD)是发生在老年期及老年前期的一种原发性退行性脑病，指的是一种持续性**神经功能活动障碍，即在没有意识障碍的状态下，记忆、思维、分析判断、视空间辨认、情绪等方面的障碍。其特征性病理变化为大脑皮层萎缩，并伴有β-淀粉样蛋白沉积，神经原纤维缠结，大量记忆性神经元数目减少，以及老年斑的形成。目前尚无特效**或逆转**进展的****。
在这篇文章中，研究人员利用老年性痴呆转基因小鼠模型研究发现，一个新型维生素B1衍生物**八周后，能显著增加老年性痴呆转基因小鼠模型在Morris水迷宫第Ⅳ象限穿台次数和停留时间，减少痴呆小鼠脑内老年斑和神经纤维缠结数量，具有剂量—效应关系。
这一实验结果表明，该新型维生素B1衍生物是通过非维生素B1依赖的作用机制发挥作用的，其药理作用与显著增加糖合酶－3α和3β的磷酸化，抑制糖合酶－3活性有关。
复旦大学附属中山医院神经内科钟春玖教授在神经系统变性**、特别是老年性痴呆与帕金森病的发病机制与神经生化、神经干细胞应用方面取得了许多成果，这一*新成果是其通过长达10年潜心研究获得。
老龄化趋势让老年性痴呆患者数量增多，因此国内外在这方面都花费了一些人力物力进行研究，但是*近的一项研究表明，阿尔茨海默氏症的基因变异并不总是有害的，它增加老年人得老年痴呆的风险，但是却能使年轻人更加聪明，具有更高的学历和比同龄人有更强的记忆力。
这个发现改善了基因变异的负面形象。它也说明了为什么这个基因变异对老年人具有破坏性的影响，但是却很常见。基因变异携带者可以在生命早期获得更有利的条件，在它的负面影响表现出来之前，允许他们生育后代，把变异基因继续传递下去。
原文检索：
Powerful beneficial effects of benfotiamine on cognitiveimpairment and {beta}-amyloid deposition in amyloid precursorprotein/presenilin-1 transgenic mice.Reduction of glucose metabolism in brain is one of the mainfeatures of Alzheimer's disease. Thiamine (vitamin B1)-dependentprocesses are critical in glucose metabolism and have been found tobe impaired in brains from patients with Alzheimer's disease.However, thiamine treatment exerts little beneficial effect inthese patients. Here, we tested the effect of benfotiamine, athiamine derivative with better bioavailability than thiamine, oncognitive impairment and pathology alterations in a mouse model ofAlzheimer's disease, the amyloid precursor protein/presenilin-1transgenic mouse. We show that after a chronic 8 week treatment,benfotiamine dose-dependently enhanced the spatial memory ofamyloid precursor protein/presenilin-1 mice in the Morris watermaze test. Furthermore, benfotiamine effectively reduced bothamyloid plaque numbers and phosphorylated tau levels in corticalareas of the transgenic mice brains. Unexpectedly, these effectswere not mimicked by another lipophilic thiamine derivative,fursultiamine, although both benfotiamine and fursultiamine wereeffective in increasing the levels of free thiamine in the brain.Most notably, benfotiamine, but not fursultiamine, significantlyelevated the phosphorylation level of glycogen synthasekinase-3alpha and -3beta, and reduced their enzymatic activities inthe amyloid precursor protein/presenilin-1 transgenic brain.Therefore, in the animal Alzheimer's disease model, benfotiamineappears to improve the cognitive function and reduce amyloiddeposition via thiamine-independent mechanisms, which are likely toinclude the suppression of glycogen synthase kinase-3 activities.These results suggest that, unlike many other thiamine-relateddrugs, benfotiamine may be beneficial for clinical Alzheimer'sdisease treatment.