Humanin: A Possible Linkage Between Alzheimer's Disease and Type 2 Diabetes

被引:15
作者
Mahboobi, Hamidreza [1 ,2 ]
Golmirzaei, Javad [3 ]
Gan, Siew H. [4 ]
Jalalian, Mehrdad [5 ]
Kamal, Mohammad A. [6 ]
机构
[1] HUMS, Infect & Trop Dis Res Ctr, Bandar Abbas, Hormozgan, Iran
[2] PNU, Tehran, Iran
[3] Shahid Beheshti Univ Med Sci, Pediat Neurol Res Ctr, Tehran, Iran
[4] Univ Sains Malaysia, Sch Med Sci, Human Genome Ctr, Kubang Kerian 16150, Kelantan, Malaysia
[5] Elect Phys Journal, Mashhad, Iran
[6] King Abdulaziz Univ, King Fahd Med Res Ctr, Jeddah 21589, Saudi Arabia
关键词
Alzheimer's disease; Amyloid beta; Apo-lipoprotein E; diabetes; inflammation; oxidative stress; ISLET AMYLOID POLYPEPTIDE; BRAIN INSULIN-RESISTANCE; RESCUE FACTOR HUMANIN; BETA-CELL APOPTOSIS; OXIDATIVE STRESS; COGNITIVE IMPAIRMENT; RISK-FACTORS; NEUROPROTECTIVE FACTOR; APOLIPOPROTEIN-E; PEPTIDE HUMANIN;
D O I
10.2174/1871527312666131223110147
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
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 anti-inflammatory drugs, such as interleukin-1 antagonists and statins, are possible drug candidates for both AD and T2DM.
引用
收藏
页码:543 / 552
页数:10
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