ReviewOxidative medicine and cellular longevity2014
Oxidative stress and metabolic syndrome: cause or consequence of Alzheimer's disease?
Review in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed.
- Examination of metabolic syndrome in Down syndrome and association with dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- What are the effects of time-restricted eating upon metabolic health outcomes in individuals with metabolic syndrome: A scoping review.Physiological reports · 2025Article
- Tau-targeting nanoparticles for treatment of Alzheimer's disease.Exploration (Beijing, China) · 2025Review
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- Article
- The Landscape of Smart Biomaterial-Based Hydrogen Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Mitochondrial dysfunction in chronic neuroinflammatory diseases (Review).International journal of molecular medicine · 2024Review
- Review
- A common molecular and cellular pathway in developing Alzheimer and cancer.Biochemistry and biophysics reports · 2024Review
- Tau Phosphorylation Patterns in the Rat Cerebral Cortex After Traumatic Brain Injury and Sodium Selenate Effects: An Epibios4rx Project 2 Study.Journal of neurotrauma · 2024Article
- Oligodendrocyte progenitor cells in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2023Review
- Alleviating the unwanted effects of oxidative stress on Aβ clearance: a review of related concepts and strategies for the development of computational modelling.Translational neurodegeneration · 2023Review
- Neuroprotective Potential and Underlying Pharmacological Mechanism of Carvacrol for Alzheimer's and Parkinson's Diseases.Current neuropharmacology · 2023Review
- Induction of Oxidative Stress in SH-SY5Y Cells by Overexpression of hTau40 and Its Mitigation by Redox-Active Nanoparticles.International journal of molecular sciences · 2022Article
- Brain Mitochondrial Dysfunction: A Possible Mechanism Links Early Life Anxiety to Alzheimer's Disease in Later Life.Aging and disease · 2022Article
- Reducing PDK1/Akt Activity: An Effective Therapeutic Target in the Treatment of Alzheimer's Disease.Cells · 2022Review
- Targeting hypercoagulation to alleviate Alzheimer's disease progression in metabolic syndrome.International journal of obesity (2005) · 2022Review
- Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function.Antioxidants (Basel, Switzerland) · 2022Article
- Naturally Occurring Antioxidant Therapy in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Bee Venom Activates the Nrf2/HO-1 and TrkB/CREB/BDNF Pathways in Neuronal Cell Responses against Oxidative Stress Induced by AβInternational journal of molecular sciences · 2022Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a major neurodegenerative disease affecting the elderly. Clinically, it is characterized by a progressive loss of memory and cognitive function. Neuropathologically, it is characterized by the presence of extracellular β-amyloid (Aβ) deposited as neuritic plaques (NP) and neurofibrillary tangles (NFT) made of abnormal and hyperphosphorylated tau protein. These lesions are capable of generating the neuronal damage that leads to cell death and cognitive failure through the generation of reactive oxygen species (ROS). Evidence indicates the critical role of Aβ metabolism in prompting the oxidative stress observed in AD patients. However, it has also been proposed that oxidative damage precedes the onset of clinical and pathological AD symptoms, including amyloid-β deposition, neurofibrillary tangle formation, vascular malfunction, metabolic syndrome, and cognitive decline. This paper provides a brief description of the three main proteins associated with the development of the disease (Aβ, tau, and ApoE) and describes their role in the generation of oxidative stress. Finally, we describe the mitochondrial alterations that are generated by Aβ and examine the relationship of vascular damage which is a potential prognostic tool of metabolic syndrome. In addition, new therapeutic approaches targeting ROS sources and metabolic support were reported.
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Registered trials
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