ReviewAntioxidants (Basel, Switzerland)2021
Diabetes and Alzheimer's Disease: Might Mitochondrial Dysfunction Help Deciphering the Common Path?
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
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Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- Recent Advances in Molecular Research on Hydrogen Sulfide (HInternational journal of molecular sciences · 2022Pooled it
- Identifying transcriptomic signatures that mediate the causal effect of genotype on Alzheimer's disease.Frontiers in neuroscience · 2026Article
- Type 3 Diabetes: Linking Insulin Resistance to Cognitive Decline.Diseases (Basel, Switzerland) · 2025Review
- From metabolic dysregulation to neurodegenerative pathology: the role of hyperglycemia, oxidative stress, and blood-brain barrier breakdown in T2D-driven Alzheimer's disease.Metabolic brain disease · 2025Review
- A systematic review on type 3 diabetes: bridging the gap between metabolic dysfunction and Alzheimer's disease.Diabetology & metabolic syndrome · 2025Review
- Serum NPTX2 and cognitive impairment in geriatric diabetes.Biomolecules & biomedicine · 2025Article
- Role and mechanism of mitochondrial dysfunction‑related gene biomarkers in the progression of type 2 diabetes mellitus.Molecular medicine reports · 2025Article
- Bridging Pancreatic Amyloidosis and Neurodegeneration: The Emerging Role of Amylin in Diabetic Dementia.International journal of molecular sciences · 2025Review
- Signs of Alzheimer's Disease: Tied to Aging.International journal of molecular sciences · 2025Review
- Impact of vitamin A on aged people's cognition and Alzheimer's disease progression in an animal model.NPJ science of food · 2025Article
- Dual Challenges in the Context of Healthy Aging: A Comprehensive Exploration of the Association between Malnutrition and Cognitive Decline in Disabled Elderly.Aging and disease · 2025Review
- Global Burden of Alzheimer's Disease Attributable to High Fasting Plasma Glucose: Epidemiological Trends and Machine Learning Insights.Risk management and healthcare policy · 2025Article
- Endogenous micropeptides as potential diagnostic biomarkers and therapeutic drugs.Frontiers in pharmacology · 2025Review
- Relationship between Alzheimer's Disease and Type 2 Diabetes: Critical Review On Cellular and Molecular Common Pathogenic Mechanisms.Current Alzheimer research · 2025Review
- Effect and mechanism of GLP-1 on cognitive function in diabetes mellitus.Frontiers in neuroscience · 2025Review
- Neuroprotective effect ofToxicology reports · 2024Article
- Identification of common biomarkers in diabetic kidney disease and cognitive dysfunction using machine learning algorithms.Scientific reports · 2024Article
- Review
- The Role of Ion-Transporting Proteins in Human Disease.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing number of clinical and epidemiological studies support the hypothesis of a tight correlation between type 2 diabetes mellitus (T2DM) and the development risk of Alzheimer's disease (AD). Indeed, the proposed definition of Alzheimer's disease as type 3 diabetes (T3D) underlines the key role played by deranged insulin signaling to accumulation of aggregated amyloid beta (Aβ) peptides in the senile plaques of the brain. Metabolic disturbances such as hyperglycemia, peripheral hyperinsulinemia, dysregulated lipid metabolism, and chronic inflammation associated with T2DM are responsible for an inefficient transport of insulin to the brain, producing a neuronal insulin resistance that triggers an enhanced production and deposition of Aβ and concomitantly contributes to impairment in the micro-tubule-associated protein Tau, leading to neural degeneration and cognitive decline. Furthermore, the reduced antioxidant capacity observed in T2DM patients, together with the impairment of cerebral glucose metabolism and the decreased performance of mitochondrial activity, suggests the existence of a relationship between oxidative damage, mitochondrial impairment, and cognitive dysfunction that could further reinforce the common pathophysiology of T2DM and AD. In this review, we discuss the molecular mechanisms by which insulin-signaling dysregulation in T2DM can contribute to the pathogenesis and progression of AD, deepening the analysis of complex mechanisms involved in reactive oxygen species (ROS) production under oxidative stress and their possible influence in AD and T2DM. In addition, the role of current therapies as tools for prevention or treatment of damage induced by oxidative stress in T2DM and AD will be debated.
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