ArticleNeurotoxicity research2020
Protective Effects of Co-administration of Zinc and Selenium Against Streptozotocin-Induced Alzheimer's Disease: Behavioral, Mitochondrial Oxidative Stress, and GPR39 Expression Alterations in Rats.
Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Synthesis, Radiochemistry, and Preclinical Assessment of the First GPR39 PET Imaging Agent.Journal of medicinal chemistry · 2026Article
- Neurotoxicity of heavy metals across the lifespan: The beneficial role of nutrition from fetus to the elderly.Advances in neurotoxicology · 2026Article
- The Effect of Zeolite Zinc on Memory Performance and Hippocampal Cell Death in a Rat Model of Alzheimer's-like Disease Induced by AβBiological trace element research · 2025Article
- GPR39 Agonist TC-G 1008 Promoted Mitochondrial Biogenesis and Improved Antioxidative Capability via CREB/PGC-1α Pathway Following Intracerebral Hemorrhage in Mice.Translational stroke research · 2025Article
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- Association between composite dietary antioxidant index and cognitive function impairment among the US older adults: a cross-sectional study based on the NHANES 2011-2014.Frontiers in nutrition · 2024Article
- Associations between plasma metal elements and risk of cognitive impairment among Chinese older adults.Frontiers in aging neuroscience · 2024Article
- Insight into the emerging and common experimental in-vivo models of Alzheimer's disease.Laboratory animal research · 2023Review
- Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Association of Dietary Intake of Zinc and Selenium with Breast Cancer Risk: A Case-Control Study in Chinese Women.Nutrients · 2023Article
- Signaling pathway mechanisms of neurological diseases induced by G protein-coupled receptor 39.CNS neuroscience & therapeutics · 2023Review
- Non-Enzymatic Antioxidants against Alzheimer's Disease: Prevention, Diagnosis and Therapy.Antioxidants (Basel, Switzerland) · 2023Review
- Intermittent theta burst stimulation attenuates oxidative stress and reactive astrogliosis in the streptozotocin-induced model of Alzheimer's disease-like pathology.Frontiers in aging neuroscience · 2023Article
- Role of micronutrients in Alzheimer's disease: Review of available evidence.World journal of clinical cases · 2022Review
- Alzheimer's Disease Association with Metals and Metalloids Concentration in Blood and Urine.International journal of environmental research and public health · 2022Article
- Silymarin-Encapsulated Xanthan Gum-Stabilized Selenium Nanocarriers for Enhanced Activity Against Amyloid Fibril Cytotoxicity.AAPS PharmSciTech · 2022Article
- Role of GPR39 in Neurovascular Homeostasis and Disease.International journal of molecular sciences · 2021Review
- Potential Effects of Melatonin and Micronutrients on Mitochondrial Dysfunction during a Cytokine Storm Typical of Oxidative/Inflammatory Diseases.Diseases (Basel, Switzerland) · 2021Review
- The Zinc-Sensing Receptor GPR39 in Physiology and as a Pharmacological Target.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Changes in the concentrations of trace metals such as zinc (Zn) and selenium (Se) can pathologically lead to neurodegenerative conditions such as the Alzheimer's disease (AD). Previous studies have shown that mitochondrial dysfunction plays an important role in the pathogenesis of AD. Several male Wistar rats were randomly divided into five groups: sham group, AD group that received 3 mg/kg of streptozotocin (STZ) intracerebroventricularly, AD + Zn group that received 10 mg/kg of Zn intraperitoneally (i.p.) for 1 week, AD + Se group that received 0.1 mg/kg of Se i.p. for 1 week, and AD + Zn + Se group that received 10 mg/kg of Zn i.p. plus 0.1 mg/kg of Se i.p. for 1 week. At end of the study, behavioral tests and mitochondrial oxidative stress and GPR39 gene expression evaluations were carried out. Co-administration of Zn and Se significantly decreased the potential collapse of mitochondrial membrane, reactive oxygen species levels, and lipid peroxidation levels while significantly increased cognitive performance, superoxide dismutase (SOD), glutathione peroxidase, and catalase activity in the brain mitochondria compared with the STZ group. In addition, no significant changes were observed in GPR39 expression in the co-treated group. Findings of the current study showed that ZnR/GPR39 receptor, mitochondrial dysfunction, and oxidative stress play important roles in the pathogenesis of AD. Co-treatment of Zn and Se improved the cognitive performance, mitochondrial dysfunction, and oxidative stress caused by STZ-induced AD. Therefore, therapeutic approaches to improve mitochondrial function could be effective in preventing the initiation and progression of AD.
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