Humanin: a possible linkage between Alzheimer's disease and type 2 diabetes
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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Humanin has demonstrated protective capacity in age-related diseases such as T2DM and Alzheimer's disease.
“Humanin has demonstrated protective capacity in age-related diseases such as T2DM and Alzheimer's disease (Mahboobi et al., 2014) and is able to restore mitochondrial function after oxidative injury in retinal pigment epithelial cells (Sreekumar et al., 2016).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Mahboobi et al., 2014
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“Growing document shows that AD is fundamentally a metabolic disease with molecular and biochemical features that correspond with diabetes mellitus and other peripheral insulin resistance disorders (Dai and Kamal 2014; de la Monte and Tong 2014; Mahboobi et al. 2014; Wang et al. 2014).”
BackgroundBreton, C. V., Song, A., Xiao, J., Kim, S., Mehta, H. H., Wan, J., Yen, K., Sioutas, C., Lurmann, F. W., Xue, S., et al. (2019) · Mitochondrion · doi:10.1016/j.mito.2019.04.001 · Cited by 106 · see citing works
“lism and cyto-protection as well as being altered in disease states (Lee et al., 2015; Mahboobi et al., 2014; Matsuoka, 2015; Xiao et al., 2016; Yen et al., 2013), providing support for a network of active mitochondrial-encoded signals that act at the cellular and organismal level.”
BackgroundMitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity
López-Lluch, G. (2017) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2016.12.005 · Cited by 103 · see citing works
“Humanin has demonstrated protective capacity in age-related diseases such as T2DM and Alzheimer’s disease (Mahboobi et al., 2014) and is able to restore mitochondrial function after oxidative injury in retinal pigment epithelial cells (Sreekumar et al., 2016).”
BackgroundPan, Y., Li, J., Lin, P., Wan, L., Qu, Y., Cao, L., & Wang, L. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1348410 · Cited by 49 · see citing works
“The increase of ceramide in the CNS activates PP2A/PKC ζ , inhibiting Akt/PKB signaling pathway.”
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“Emerging evidence suggests that changes in the delicate balance of neurotransmitters inside the brain can play a key role in the development and progression of diabetes and Alzheimer’s disease [83].”
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Self-citationZhang, H., Cao, Y., Pei, H., Wang, H., Ma, L., Wang, Z., Diao, X., Yang, Y., Liu, N., Wei, Y., et al. (2020) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2020/8312347 · Cited by 15 · see citing works
“+e inclusion criteria were as follows: (1) age between 50 and 85 years; (2) fulfillment of diagnostic criteria for VaD according to the Diagnostic and Statistical Manual of Mental Disorders [26] and the National Institute of Neurological Disorders and Stroke [27]; (3) Clinical Dementia Rating (CDR) score of 1 or 2 (de…”
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“In this context, the recent discovery of (i) humanin, a mitochondria-derived peptide expressing neuro-metabotrophic effects (29,30), and (ii) irisin, a myokine/ adipokine involved in the browning of WAT (31,32), may lead to the development of a novel approach in therapy for Homo diabesus.”
BackgroundHomo diabesus: involvement of metabotrophic factors
Aloe, L., Tonchev, A. B., Fiore, M., et al. (2013) · Adipobiology · doi:10.14748/adipo.v5.297 · Cited by 10 · see citing works
“context, the recent discovery of (i) humanin, a mitochondriaderived peptide expressing neuro- and metabotrophic effect (29,30), and (ii) irisin, a myokine/adipokine involved in the browning of WAT (31,32), may open a further perspective for the therapy of Homo diabesus.”
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“Furthermore, AD and T2DM have several pathophysiological pathways in common [3].”
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Shan, Y., Liu, X., Ge, W., et al. (2026) · Toxicology and Industrial Health · doi:10.1177/07482337261445494
“The decrease in HN content in AD indicates that oxidative stress is an important factor in neuronal degenerative damage (Mahboobi et al., 2014).”
- Authors
- Mahboobi, H., Golmirzaei, J., Gan, S., Jalalian, M., & Kamal, M.
- Affiliations
- Hormozgan University of Medical Sciences (IR)
- Corresponding author
- Kamal, Mohammad
- Venue
- CNS & Neurological Disorders - Drug Targets
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2014-05-31
- Volume
- 13
- Issue
- 3
- Pages
- 543-552
- ISSN
- 1568-007X (ISSN-L)
- 1871-5273
- OpenAlex
- W2157357302
- Cited by
- 21
- References
- 0
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 1 · 2022: 2 · 2020: 2 · 2019: 2 · 2018: 1 · 2016: 1 · 2015: 1 · 2014: 7 · 2013: 1
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- CNS & Neurological Disorders - Drug Targets (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- humanin, Alzheimer's disease, type 2 diabetes, insulin resistance, oxidative stress, amyloid deposition, advanced glycation end products, lipid metabolism disorders, low-grade inflammation, mitochondrial peptides, neuroprotection, IL-1 inhibitors, statins, nonsteroidal anti-inflammatory drugs
- MeSH terms
- Alzheimer Disease, Apolipoproteins E, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Oxidative Stress, Intracellular Signaling Peptides and Proteins
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