Department of Pharmaceutical Quality Assurance, SSR College of Pharmacy, Sayli, Silvassa-396230, India.
SSR College of Pharmacy, Silvassa, India.
Curr Diabetes Rev. 2022;18(8):e131221198790. doi: 10.2174/1573399818666211213103624.
According to research, Alzheimer's disease (AD) is considered a metabolic illness caused by defective insulin signaling, insulin resistance, and low insulin levels in the brain. Type 3 diabetes has been postulated for AD because reduced insulin signaling has molecular and physiological consequences that are comparable to type I and type 2 diabetes mellitus, respectively. The similarities between type 2 diabetes and Alzheimer's disease suggest that these clinical trials might yield therapeutic benefits. However, it is important to note that lowering your risk of Alzheimer's dementia, whether you have diabetes or not, is still a multidimensional process involving factors like exercise, smoking, alcohol, food, and mental challenges. The current aim is to show that the relationship between T3D and AD is based on both the processing of amyloid-β (Aβ) precursor protein toxicity and the clearance of Aβ, which are the results of impaired insulin signaling. The brain's metabolism, with its high lipid content and energy needs, places excess demands on mitochondria and appears more susceptible to oxidative damage than the rest of the body. Current data suggests that increased oxidative stress relates to amyloid-β (Aβ) pathology and the onset of AD.
根据研究,阿尔茨海默病(AD)被认为是一种代谢疾病,由胰岛素信号转导缺陷、胰岛素抵抗和大脑中胰岛素水平低引起。有人提出 AD 是 3 型糖尿病,因为降低胰岛素信号转导具有与 I 型和 II 型糖尿病分别相当的分子和生理后果。2 型糖尿病和阿尔茨海默病之间的相似性表明,这些临床试验可能会产生治疗益处。然而,需要注意的是,无论是否患有糖尿病,降低患阿尔茨海默病痴呆的风险仍然是一个多方面的过程,涉及运动、吸烟、饮酒、饮食和心理挑战等因素。目前的目的是表明 T3D 与 AD 之间的关系基于淀粉样蛋白-β(Aβ)前体蛋白毒性的处理和 Aβ的清除,这是胰岛素信号转导受损的结果。大脑的新陈代谢具有高脂质含量和能量需求,对线粒体的要求过高,比身体其他部位更容易受到氧化损伤。目前的数据表明,氧化应激增加与淀粉样蛋白-β(Aβ)病理学和 AD 的发生有关。