神经保护
发病机制
糖基化
氧化应激
2型糖尿病
胰岛素抵抗
2型糖尿病
炎症
医学
糖尿病
阿尔茨海默病
β淀粉样蛋白
疾病
生物信息学
内分泌学
药理学
内科学
生物
作者
Hamidreza Mahboobi,Javad Golmirzaei,Siew Hua Gan,Mehrdad Jalalian,Mohammad Amjad Kamal
出处
期刊:Cns & Neurological Disorders-drug Targets
[Bentham Science]
日期:2014-05-31
卷期号:13 (3): 543-552
被引量:19
标识
DOI:10.2174/1871527312666131223110147
摘要
The prevalence of Alzheimer’s disease (AD) is higher among type 2 diabetes mellitus (T2DM) patients. In T2DM patients, the progression of AD is more rapid. Furthermore, several pathophysiological pathways are common to AD and T2DM. Humanin is a recently introduced, mitochondrial-derived peptide with neuroprotective effects. Humanin can alter the mechanisms involved in AD and T2DM pathogenesis. Insulin resistance as well as oxidative stress has been shown to be associated with increased amyloid deposition in brain neurons and islet beta cells. Moreover, advanced glycation end products and lipid metabolism disorders are common pathways of oxidative stress and low-grade systemic inflammation in AD and T2DM. These common pathways may explain AD and T2DM pathogenesis and suggest common treatments for both diseases. Treatments for T2DM and AD attempt to slow cognitive decline, and recent investigations have focused on agents that may alter pathways common to AD and T2DM pathogenesis. Non-steroidal antiinflammatory drugs, such as interleukin-1 antagonists and statins, are possible drug candidates for both AD and T2DM. Keywords: Alzheimer's disease, Amyloid beta, Apo-lipoprotein E, diabetes, inflammation, oxidative stress.
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