Alzheimer’s disease as type 3 diabetes: understanding the link and implications
Open accessAbstract
Alzheimer’s disease (AD) and type 2 diabetes mellitus (T2DM) are two prevalent conditions that present considerable public health issue in aging populations worldwide. Recent research has proposed a novel conceptualization of AD as “type 3 diabetes”, highlighting the critical roles of insulin resistance and impaired glucose metabolism in the pathogenesis of the disease. This article examines the implications of this association, exploring potential new avenues for treatment and preventive strategies for AD. Key evidence linking diabetes to AD emphasizes critical metabolic processes that contribute to neurodegeneration, including inflammation, oxidative stress, and alterations in insulin signaling pathways. By framing AD within this metabolic context, we can enhance our understanding of its etiology, which in turn may influence early diagnosis, treatment plans, and preventive measures. Understanding AD as a manifestation of diabetes opens up the possibility of employing novel therapeutic strategies that incorporate lifestyle modifications and the use of antidiabetic medications to mitigate cognitive decline. This integrated approach has the potential to improve patient outcomes and deepen our comprehension of the intricate relationship between neurodegenerative diseases and metabolic disorders.
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People with Alzheimer disease or other dementias are more likely to develop diabetes than those without it.
“People with Alzheimer disease or other dementias are more likely to develop diabetes than those without it; this possible link emphasizes critical metabolic processes that contribute to neurodegeneration (21).”
From 13. Older Adults: Standards of Care in Diabetes—2026 (2026) · cites this paper as [21]
The Introduction and section 4.1 discuss whether people with diabetes are more likely to develop Alzheimer’s disease or other dementias—the reverse of the claimed direction. A search for diabetes developing after an Alzheimer’s or dementia diagnosis found no passage addressing that comparison. The paper’s discussion of shared metabolic processes does not establish the claimed risk. (LLM, conf=0.76)
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- Authors
- Kciuk, M., Kruczkowska, W., Gałęziewska, J., Wanke, K., Kałuzińska-Kołat, Ż., Aleksandrowicz, M., & Kontek, R.
- Affiliations
- University of Łódź (PL)
- Medical University of Lodz (PL)
- Department of Functional Genomics, Medical University of Lodz, 90-752 Lodz, Poland
- Mossakowski Medical Research Institute, Polish Academy of Sciences (PL)
- Corresponding author
- Kciuk, Mateusz
- ORCID
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2024-11-07
- Volume
- 25
- Issue
- 22
- Pages
- 11955
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC11593477
- OpenAlex
- W4404148136
- Cited by
- 98
- References
- 302
- Citations by year
- 2026: 53 · 2025: 45
- FWCI
- 5.59
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- 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, type 3 diabetes, type 2 diabetes, insulin resistance, impaired glucose metabolism, insulin signaling, neuroinflammation, oxidative stress, cognitive decline, antidiabetic drugs, lifestyle modification, Alzheimer's disease prevention, Alzheimer's disease treatment
- MeSH terms
- Alzheimer Disease, Animals, Diabetes Mellitus, Type 2, Humans, Insulin, Insulin Resistance, Oxidative Stress
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