Kroner Zina
American Board of Internal Medicine, USA.
Altern Med Rev. 2009 Dec;14(4):373-9.
In recent years, Alzheimer's disease (AD) has been considered to be, in part, a neuroendocrine disorder, even referred to by some as type 3 diabetes. Insulin functions by controlling neurotransmitter release processes at the synapses and activating signaling pathways associated with learning and long-term memory. Novel research demonstrates that impaired insulin signaling may be implicated in AD. Post-mortem brain studies show that insulin expression is inversely proportional to the Braak stage of AD progression. It was also demonstrated that neurotoxins, coined amyloid beta-derived diffusible ligands (ADDLs), disrupt signal transduction at synapses, making the cell insulin resistant. ADDLs reduce plasticity of the synapse, potentiate synapse loss, contribute to oxidative damage, and cause AD-type tau hyperphosphorylation. Diabetes and AD have signs of increased oxidative stress in common, including advanced glycation end products (AGEs), when compared to normal subjects. Diabetic patients appear to have an increased risk for AD because AGEs accumulate in neurofibrillary tangles and amyloid plaques in AD brains. This research should encourage a more proactive approach to early diagnosis of diabetes and nutritional counseling for AD patients.
近年来，阿尔茨海默病（AD）部分被认为是一种神经内分泌紊乱，甚至被一些人称为3型糖尿病。胰岛素通过控制突触处的神经递质释放过程和激活与学习及长期记忆相关的信号通路发挥作用。新的研究表明，胰岛素信号受损可能与AD有关。死后脑部研究表明，胰岛素表达与AD进展的Braak阶段成反比。研究还表明，被称为淀粉样β衍生可扩散配体（ADDLs）的神经毒素会破坏突触处的信号转导，使细胞产生胰岛素抵抗。ADDLs会降低突触可塑性，加剧突触丧失，导致氧化损伤，并引起AD型tau蛋白过度磷酸化。与正常受试者相比，糖尿病和AD都有氧化应激增加的迹象，包括晚期糖基化终产物（AGEs）。糖尿病患者患AD的风险似乎更高，因为AGEs在AD大脑的神经纤维缠结和淀粉样斑块中积累。这项研究应鼓励采取更积极主动的方法对糖尿病进行早期诊断，并为AD患者提供营养咨询。
