ArticleMolecular neurobiology2020
Gold Nanoparticles Treatment Reverses Brain Damage in Alzheimer's Disease Model.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 137 citations in OpenAlex.
- Unlocking the potential of gold nanoparticles with insights into green synthesis, mechanisms, characterization and multifunctional applications.Discover nano · 2026Review
- The central role of mitochondrial dysfunction in neurodegeneration: implications for therapy.Molecular and cellular biochemistry · 2026Review
- Nanoparticles that target nonamyloid and nontau pathways in Alzheimer's disease.Discover nano · 2026Review
- The therapeutic efficacy of nanoparticles in the treatment of alzheimer's disease.Acta neurologica Belgica · 2026Review
- Heterotrimetallic Au@CuMaterials today. Bio · 2026Article
- Low-Dimensional Nanomaterials in Alzheimer's Disease: Current Applications.Current Alzheimer research · 2026Review
- Toward nanomedicine-enabled RNA therapeutics for Alzheimer's disease.Molecular neurodegeneration advances · 2026Review
- Systemic administration of gold nanoparticles attenuates anxiety-related behaviors and enhances spatial learning performance in rats.IBRO neuroscience reports · 2025Article
- Advances in Gold Nanoparticles for the Diagnosis and Management of Alzheimer's Disease.Pharmaceutics · 2025Review
- Nanomedicine: a cost-effective and powerful platform for managing neurodegenerative diseases.Metabolic brain disease · 2025Review
- The blood-brain barriers: novel nanocarriers for central nervous system diseases.Journal of nanobiotechnology · 2025Review
- Mitochondria targeted nanoparticles for the treatment of mitochondrial dysfunction-associated brain disorders.Frontiers in bioengineering and biotechnology · 2025Review
- Non-pharmacological treatment of Alzheimer's disease: an update.Frontiers in aging neuroscience · 2025Review
- Review
- Gold Nanoparticles in Neurological Diseases: A Review of Neuroprotection.International journal of molecular sciences · 2024Review
- Biomaterials-based anti-inflammatory treatment strategies for Alzheimer's disease.Neural regeneration research · 2024Review
- Green synthesis of nanoparticles using medicinal plants as an eco-friendly and therapeutic potential approach for neurodegenerative diseases: a comprehensive review.Frontiers in neuroscience · 2024Review
- Nano biomaterials based strategies for enhanced brain targeting in the treatment of neurodegenerative diseases: an up-to-date perspective.Journal of nanobiotechnology · 2023Review
- Role of Nanoparticle-Conjugates and Nanotheranostics in Abrogating Oxidative Stress and Ameliorating Neuroinflammation.Antioxidants (Basel, Switzerland) · 2023Review
- Current Overview of Metal Nanoparticles' Synthesis, Characterization, and Biomedical Applications, with a Focus on Silver and Gold Nanoparticles.Pharmaceuticals (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is characterized by amyloid (A)β peptide accumulation and intracellular neurofibrillary tangles. New hypotheses have suggested that AD involves neuroinflammation and oxidative stress. Gold nanoparticles (AuNP) presents anti-inflammatory and antioxidant characteristics. The present study evaluated the AuNP treatment on an AD model (okadaic acid, OA). Male Wistar rats were injected intracerebroventricularly with OA (100 μg); 24 h later they were treated with 20-nm AuNP (at a dose 2.5 mg/kg) every 48 h for 21 days. The following groups were separated (n = 12/group): Sham, AuNP, OA, and OA + AuNP. OA increases Tau phosphorylation in the cortex and hippocampus, while AuNP treatment maintained it as normal. Spatial memory was impaired by OA, and AuNP treatment prevented this deficit. Neurotrophic factors (BDNF and NGF- β) in the cortex and hippocampus were decreased by OA. The OA and OA + AuNP groups showed increased interleukin (IL)-1 β in the hippocampus and cortex, and the AuNP group showed increased IL-1 β in the hippocampus. In both groups, S100 levels in the cortex and hippocampus were increased by OA. IL-4 was increased in OA + AuNP animals. AuNPs prevented oxidative stress (sulfhydryl and nitrite levels) in brain structures induced by OA. Moreover, OA modulated ATP synthase activity, and AuNP maintained normal brain mitochondrial function. The antioxidant capacities were reduced by OA, and AuNP restored antioxidant status (SOD, catalase activities and GSH levels) on brain. OA-induced damage on brain tissues, and long-term AuNP treatment prevented the neuroinflammation, modulation of mitochondrial function, and impaired cognition induced by AD model, showing that AuNPs may be a promising treatment for neurodisease caused by these elements.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.