ArticleEvidence-based complementary and alternative medicine : eCAM2015
The Protective Effects of Areca catechu Extract on Cognition and Social Interaction Deficits in a Cuprizone-Induced Demyelination Model.
Article in Evidence-based complementary and alternative medicine : eCAM, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Multi-Targeted Neuroprotection byInternational journal of molecular sciences · 2026Article
- The multistep progression of areca nut-induced oral cancer: a mechanistic roadmap from pathogenesis to precision therapy.Life medicine · 2026Review
- Potential therapeutic effects of ibudilast and retinoic acid against cuprizone-induced behavioral and biochemical changes in mouse brain.Frontiers in molecular neuroscience · 2025Article
- Biochanin A Improves Memory Decline and Brain Pathology in Cuprizone-Induced Mouse Model of Multiple Sclerosis.Behavioral sciences (Basel, Switzerland) · 2022Article
- Dietary Supplementation WithFrontiers in neuroscience · 2022Article
- Metformin Therapy Attenuates Pro-inflammatory Microglia by Inhibiting NF-κB in Cuprizone Demyelinating Mouse Model of Multiple Sclerosis.Neurotoxicity research · 2021Article
- Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801-Induced Mouse Model of Schizophrenia.Frontiers in psychiatry · 2020Article
- Traditional Chinese Medicine Decoction Combined With Antipsychotic for Chronic Schizophrenia Treatment: A Systematic Review and Meta-analysis.Frontiers in pharmacology · 2020Review
- Arecoline attenuates memory impairment and demyelination in a cuprizone-induced mouse model of schizophrenia.Neuroreport · 2019Article
- Low Field Magnetic Stimulation Ameliorates Schizophrenia-Like Behavior and Up-Regulates Neuregulin-1 Expression in a Mouse Model of Cuprizone-Induced Demyelination.Frontiers in psychiatry · 2018Article
- Role of Plant Derived Alkaloids and Their Mechanism in Neurodegenerative Disorders.International journal of biological sciences · 2018Review
- Olig2 Silence Ameliorates Cuprizone-Induced Schizophrenia-Like Symptoms in Mice.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Transplanted miR-219-overexpressing oligodendrocyte precursor cells promoted remyelination and improved functional recovery in a chronic demyelinated model.Scientific reports · 2017Article
- Cyclin-dependent kinase inhibitor flavopiridol promotes remyelination in a cuprizone induced demyelination model.Cell cycle (Georgetown, Tex.) · 2016Article
- Identifying Plant-Human Disease Associations in Biomedical Literature: A Case Study.AMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schizophrenia is a serious psychiatric illness with an unclear cause. One theory is that demyelination of white matter is one of the main pathological factors involved in the development of schizophrenia. The current study evaluated the protective effects of Areca catechu nut extract (ANE) on a cuprizone-induced demyelination mouse model. Two doses of ANE (1% and 2%) were administered orally in the diet for 8 weeks. Animals subjected to demyelination showed impaired spatial memory and less social activity. In addition, mice subjected to demyelination displayed significant myelin damage in cortex and demonstrated a higher expression of NG2 and PDGFRα and AMPK activation. ANE treatment not only significantly enhanced cognitive ability and social activity, but also protected myelin against cuprizone toxicity by promoting oligodendrocyte precursor cell (OPC) differentiation. In addition, ANE treatment demonstrated significant dephosphorylation of AMPKα, indicating a regulatory role for ANE in schizophrenia. This study showed that ANE treatment may enhance cognitive ability and social activity by facilitating OPC differentiation and protecting against myelin damage in cortex. Results also suggest the AMPK signaling pathway may be involved in this process.
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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.