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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