Possible Implications of Insulin Resistance and Glucose Metabolism in Alzheimer's Disease Pathogenesis
Open accessAbstract
Type 2 diabetes mellitus (DM) appears to be a significant risk factor for Alzheimer disease (AD). Insulin and insulin-like growth factor-1 (IGF-1) also have intense effects in the central nervous system (CNS), regulating key processes such as neuronal survival and longevity, as well as learning and memory. Hyperglycaemia induces increased peripheral utilization of insulin, resulting in reduced insulin transport into the brain. Whereas the density of brain insulin receptor decreases during age, IGF-1 receptor increases, suggesting that specific insulin-mediated signals is involved in aging and possibly in cognitive decline. Molecular mechanisms that protect CNS neurons against β-amyloid-derived-diffusible ligands (ADDL), responsible for synaptic deterioration underlying AD memory failure, have been identified. The protection mechanism does not involve simple competition between ADDLs and insulin, but rather it is signalling dependent down-regulation of ADDL-binding sites. Defective insulin signalling make neurons energy deficient and vulnerable to oxidizing or other metabolic insults and impairs synaptic plasticity. In fact, destruction of mitochondria, by oxidation of a dynamic-like transporter protein, may cause synapse loss in AD. Moreover, interaction between Aβ and τ proteins could be cause of neuronal loss. Hyperinsulinaemia as well as complete lack of insulin result in increased τ phosphorylation, leading to an imbalance of insulin-regulated τ kinases and phosphatates. However, amyloid peptides accumulation is currently seen as a key step in the pathogenesis of AD. Inflammation interacts with processing and deposit of β-amyloid. Chronic hyperinsulinemia may exacerbate inflammatory responses and increase markers of oxidative stress. In addition, insulin appears to act as 'neuromodulator', influencing release and reuptake of neurotransmitters, and improving learning and memory. Thus, experimental and clinical evidence show that insulin action influences cerebral functions. In this paper, we reviewed several mechanisms by which insulin may affect pathophysiology in AD.
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Insulin resistance has been found in association with Alzheimer's disease independently of coincident type 2 diabetes mellitus.
“Insulin resistance has also been found in association with AD independently on coincident T2DM (Bosco et al., 2011).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Bosco et al., 2011
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- Authors
- Bosco, D., Fava, A., Plastino, M., Montalcini, T., & Pujia, A.
- Affiliations
- Magna Graecia University (IT)
- Corresponding author
- Bosco, Domenico
- Venue
- Journal of Cellular and Molecular Medicine
- Publisher
- Wiley
- Published
- 2011-08-28
- Volume
- 15
- Issue
- 9
- Pages
- 1807-1821
- ISSN
- 1582-1838 (ISSN-L)
- PMC
- PMC3918038
- OpenAlex
- W2005398842
- Cited by
- 283
- References
- 179
- Citations by year
- 2026: 13 · 2025: 21 · 2024: 18 · 2023: 20 · 2022: 18 · 2021: 16 · 2020: 18 · 2019: 19 · 2018: 12 · 2017: 24 · 2016: 12 · 2015: 16 · 2014: 29 · 2013: 22 · 2012: 21
- FWCI
- 2.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cellular and Molecular Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (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
- Alzheimer's disease, insulin resistance, glucose metabolism, type 2 diabetes, insulin-like growth factor I, IGF-1 receptor, hyperglycemia, tau phosphorylation, hyperinsulinemia, oxidative stress, neuroinflammation, mitochondrial dysfunction, synaptic plasticity, synaptic loss, learning and memory, insulin signaling
- MeSH terms
- Alzheimer Disease, Brain, Glucose, Humans, Insulin Resistance, Signal Transduction, Oxidative Stress
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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