Abstract
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.
CNS & Neurological Disorders - Drug Targets
Title:Humanin: A Possible Linkage Between Alzheimer’s Disease and Type 2 Diabetes
Volume: 13 Issue: 3
Author(s): Hamidreza Mahboobi, Javad Golmirzaei, Siew H. Gan, Mehrdad Jalalian and Mohammad A. Kamal
Affiliation:
Keywords: Alzheimer's disease, Amyloid beta, Apo-lipoprotein E, diabetes, inflammation, oxidative stress.
Abstract: 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.
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Cite this article as:
Mahboobi Hamidreza, Golmirzaei Javad, Gan H. Siew, Jalalian Mehrdad and Kamal A. Mohammad, Humanin: A Possible Linkage Between Alzheimer’s Disease and Type 2 Diabetes, CNS & Neurological Disorders - Drug Targets 2014; 13 (3) . https://dx.doi.org/10.2174/1871527312666131223110147
DOI https://dx.doi.org/10.2174/1871527312666131223110147 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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