ArticleBrain research2010
An okadaic acid-induced model of tauopathy and cognitive deficiency.
Article in Brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 77 citations in OpenAlex.
- From Tradition to Translation: A Critical Appraisal ofInternational journal of molecular sciences · 2026Review
- Sub-Neuronal Network Profiling of Extracellular Vesicle Release Using a Compartmentalized Neurofluidic Platform.Advanced biology · 2026Article
- Tau protein in Parkinson's disease: advances in phosphoproteomics and molecular dynamics simulations.Frontiers in aging neuroscience · 2026Review
- Amelioration of Alzheimer's Disease Pathology in Zebrafish by Photobiomodulation.Biomedicines · 2025Article
- Discovery of a brain penetrant SGK1 inhibitor using a ligand- and structure-based virtual screening methodology.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Ideal animal models according to multifaceted mechanisms and peculiarities in neurological disorders: present and challenges.Archives of pharmacal research · 2025Review
- Exploring the molecular mechanisms underlying neuroprotective effect of ellagic acid in okadaic acid-induced Alzheimer's phenotype.Metabolic brain disease · 2024Article
- Article
- Impaired Dopamine Release and Latent Learning in Alzheimer's Disease Model Zebrafish.ACS chemical neuroscience · 2022Article
- Alzheimer's Disease and Toxins Produced by Marine Dinoflagellates: An Issue to Explore.Marine drugs · 2022Review
- Experimentally induced animal models for cognitive dysfunction and Alzheimer's disease.MethodsX · 2022Review
- Neuroprotective Studies of Evodiamine in an Okadaic Acid-Induced Neurotoxicity.International journal of molecular sciences · 2021Article
- Melatonin Rescues the Dendrite Collapse Induced by the Pro-Oxidant Toxin Okadaic Acid in Organotypic Cultures of Rat Hilar Hippocampus.Molecules (Basel, Switzerland) · 2020Article
- Gold Nanoparticles Treatment Reverses Brain Damage in Alzheimer's Disease Model.Molecular neurobiology · 2020Article
- Screening of tau protein kinase inhibitors in a tauopathy-relevant cell-based model of tau hyperphosphorylation and oligomerization.PloS one · 2020Article
- Novel Peptidomic Approach for Identification of Low and High Molecular Weight Tauopathy Peptides Following Calpain Digestion, and Primary Culture Neurotoxic Challenges.International journal of molecular sciences · 2019Article
- The insect, Galleria mellonella, is a compatible model for evaluating the toxicology of okadaic acid.Cell biology and toxicology · 2019Article
- The GSK3β inhibitor, TDZD-8, rescues cognition in a zebrafish model of okadaic acid-induced Alzheimer's disease.Neurochemistry international · 2019Article
- Lanthionine ketimine-5-ethyl ester provides neuroprotection in a zebrafish model of okadaic acid-induced Alzheimer's disease.Neurochemistry international · 2018Article
- Original Research: Influence of okadaic acid on hyperphosphorylation of tau and nicotinic acetylcholine receptors in primary neurons.Experimental biology and medicine (Maywood, N.J.) · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease that causes cognitive and behavioral deterioration in the elderly. Neurofibrillary tangles (NFTs) are one of the pathological hallmarks of AD that has been shown to correlate positively with the severity of dementia in the neocortex of AD patients. In an attempt to characterize an in vivo AD tauopathy model, okadaic acid (OA), a protein phosphatase inhibitor, was microinfused into the right lateral dorsal hippocampus area of ovariectomized adult rat. Cognitive deficiency was seen in OA-treated rats without a change in motor function. Both silver staining and immunohistochemistry staining revealed that OA treatment induces NFTs-like conformational changes in both the cortex and hippocampus. Phosphorylated tau as well as cyclin-dependent kinase 5 (cdk5) and its coactivator, p25, were significantly increased in these regions of the brain. Oxidative stress was also increased with OA treatment as measured by protein carbonylation and lipid peroxidation. These data suggest that the unilateral microinfusion of OA into the dorsal hippocampus causes cognitive deficiency, NFTs-like pathological changes, and oxidative stress as seen in AD pathology via tau hyperphosphorylation caused by inhibition of protein phosphatases.
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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.