ReviewMolecular neurobiology2014
Molecular and cellular mechanism of okadaic acid (OKA)-induced neurotoxicity: a novel tool for Alzheimer's disease therapeutic application.
Review in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.
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Who cites it
57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 108 citations in OpenAlex.
- Glucagon-like peptide 1 (GLP-1) receptor agonists in experimental Alzheimer's disease models: a systematic review and meta-analysis of preclinical studies.Frontiers in pharmacology · 2023Pooled it
- The cellular model for Alzheimer's disease research: PC12 cells.Frontiers in molecular neuroscience · 2022Pooled it
- Vitamin B6 Modifies Tau-Induced Cellular Stress- and Proteostasis-Related Responses.Journal of fungi (Basel, Switzerland) · 2026Article
- The neuroprotective effect of Cucurbitacin B against Aβ and tau toxicities requires functional HDAC6 and stress granule pathways.Biogerontology · 2026Article
- Brain Permeable SGK1 Inhibitors: A Promising Therapeutic Strategy for Neurodegenerative Diseases.Journal of medicinal chemistry · 2026Article
- Sub-Neuronal Network Profiling of Extracellular Vesicle Release Using a Compartmentalized Neurofluidic Platform.Advanced biology · 2026Article
- ZDWX-25, a dual DYRK1A/GSK3β inhibitor, attenuates tau hyperphosphorylation and neuroinflammation in acute mouse models.Frontiers in pharmacology · 2026Article
- Diarrhetic Shellfish Poisoning Toxins: Current Insights into Toxicity, Mechanisms, and Ecological Impacts.Marine drugs · 2025Review
- 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
- Sea Squirt-Derived Peptide WLP Mitigates OKA-Induced Alzheimer's Disease-like Phenotypes in Human Cerebral Organoid.Antioxidants (Basel, Switzerland) · 2025Article
- Comparative Study of Injected Alzheimer's Disease Models in Rats: Insights from Experimental Research.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Article
- Exploring the molecular mechanisms underlying neuroprotective effect of ellagic acid in okadaic acid-induced Alzheimer's phenotype.Metabolic brain disease · 2024Article
- Identification and immunological characterization of genes associated with ferroptosis in Alzheimer's disease and experimental demonstration.Molecular medicine reports · 2024Article
- The protective effects of protocatechuic acid against natural and chemical toxicants: cellular and molecular mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Article
- Role of Tau Protein in Neurodegenerative Diseases and Development of Its Targeted Drugs: A Literature Review.Molecules (Basel, Switzerland) · 2024Review
- Insight into the emerging and common experimental in-vivo models of Alzheimer's disease.Laboratory animal research · 2023Review
- Urolithin A exhibits a neuroprotective effect against Alzheimer's disease by inhibiting DYRK1A activity.Journal of food and drug analysis · 2023Article
- The Cell Transformation Assay: A Historical Assessment of Current Knowledge of Applications in an Integrated Approach to Testing and Assessment for Non-Genotoxic Carcinogens.International journal of molecular sciences · 2023Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Okadaic acid (OKA), a polyether C38 fatty acid toxin extracted from a black sponge Hallichondria okadaii, is a potent and selective inhibitor of protein phosphatase, PP1 and PP2A. OKA has been proved to be a powerful probe for studying the various regulatory mechanisms and neurotoxicity. Because of its property to inhibit phosphatase activity, OKA is associated with protein phosphorylation; it is implicated in hyperphosphorylation of tau and in later stages causes Alzhiemer's disease (AD)-like pathology. AD is a progressive neurodegenerative disorder, pathologically characterized by extracellular amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles (NFTs). The density of tau tangles in AD pathology is associated with cognitive dysfunction. Recent studies have highlighted the importance of serine/threonine protein phosphatases in many processes including apoptosis and neurotoxicity. Although OKA causes neurotoxicity by various pathways, the exact mechanism is still not clear. The activation of major kinases, such as Ser/Thr, MAPK, ERK, PKA, JNK, PKC, CaMKII, Calpain, and GSK3β, in neurons is associated with AD pathology. These kinases, associated with abnormal hyperphosphorylation of tau, suggest that the cascade of these kinases could exclusively be involved in the pathogenesis of AD. The activity of serine/threonine protein phosphatases needs extensive study as these enzymes are potential targets for novel therapeutics with applications in many diseases including cancer, inflammatory diseases, and neurodegeneration. There is a need to pay ample attention on MAPK kinase pathways in AD, and OKA can be a better tool to study cellular and molecular mechanism for AD pathology. This review elucidates the regulatory mechanism of PP2A and MAPK kinase and their possible mechanisms involved in OKA-induced apoptosis, neurotoxicity, and AD-like pathology.
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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.