ArticleProceedings of the National Academy of Sciences of the United States of America2009
Overexpression of SOD-2 reduces hippocampal superoxide and prevents memory deficits in a mouse model of Alzheimer's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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Who cites it
113 citing papers in PubMed, 222 citations in OpenAlex.
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- Gene-Exercise Interactions in Amyloid Metabolism and Clearance: Implications for Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Functional Specificity of Astrocyte Subtypes in Alzheimer's Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data.Molecular neurobiology · 2025Article
- Bridging the molecular and clinical aspects of resveratrol in Alzheimer's disease: a review.3 Biotech · 2025Review
- Proteins with cognition-associated structural changes in a rat model of aging exhibit reduced refolding capacity.Science advances · 2025Article
- Manganese Superoxide Dismutase: Structure, Function, and Implications in Human Disease.Antioxidants (Basel, Switzerland) · 2025Review
- The Role of Astrocytes in Synaptic Dysfunction and Memory Deficits in Alzheimer's Disease.Biomolecules · 2025Review
- Superoxide dismutase is associated with cerebral small vessel disease burden and vascular mild cognitive impairment in elderly patients.Frontiers in neuroscience · 2025Article
- Insufficient Sleep and Alzheimer's Disease: Potential Approach for Therapeutic Treatment Methods.Brain sciences · 2024Review
- Effects silymarin and rosuvastatin on amyloid-carriers level in dyslipidemic Alzheimer's patients: A double-blind placebo-controlled randomized clinical trial.IBRO neuroscience reports · 2024Article
- Mouse models used to test the role of reactive oxygen species in aging and age-related chronic diseases.Free radical biology & medicine · 2024Review
- Exploring the Role of Reactive Oxygen Species in the Pathogenesis and Pathophysiology of Alzheimer's and Parkinson's Disease and the Efficacy of Antioxidant Treatment.Antioxidants (Basel, Switzerland) · 2024Review
- Emerging Functional Connections Between Metabolism and Epigenetic Remodeling in Neural Differentiation.Molecular neurobiology · 2024Review
- Superoxide dismutase and neurological disorders.IBRO neuroscience reports · 2024Review
- Mitochondria-Targeted Antioxidant Therapeutics for Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2024Review
- The Bioactivity and Phytochemicals ofInternational journal of molecular sciences · 2024Review
- Role of oxidative stress in neurodegenerative disorders: a review of reactive oxygen species and prevention by antioxidants.Brain communications · 2024Review
- Disorders of Endogenous and Exogenous Antioxidants in Neurological Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Direct Evidence for UsingAntioxidants (Basel, Switzerland) · 2023Article
53 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease characterized by impaired cognitive function and the deposition of extracellular amyloid plaques and intracellular tangles. Although the proximal cause of AD is not well understood, it is clear that amyloid-beta (Abeta) plays a critical role in AD pathology. Recent studies also implicate mitochondrial abnormalities in AD. We investigated this idea by crossing mice that overexpress mitochondrial superoxide dismutase (SOD-2) with the Tg2576 mouse model of AD that overexpresses the human amyloid precursor protein carrying the Swedish mutation (K670N:M671L). We found that overexpression of SOD-2 decreased hippocampal superoxide, prevented AD-related learning and memory deficits, and reduced Abeta plaques. Interestingly, SOD-2 overexpression did not affect the absolute levels of Abeta(1-40) and Abeta(1-42), but did significantly reduce the Abeta(1-42) to Abeta(1-40) ratio, thereby shifting the balance toward a less amyloidogenic Abeta composition. These findings directly link mitochondrial superoxide to AD pathology and demonstrate the beneficial effects of a mitochondrial anti-oxidant enzyme, hence offering significant therapeutic implications for AD.
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Registered trials
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