ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Enhanced tau phosphorylation in the hippocampus of mice treated with 3,4-methylenedioxymethamphetamine ("Ecstasy").
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Cognitive Effects of MDMA in Laboratory Animals: A Systematic Review Focusing on Dose.Pharmacological reviews · 2019Pooled it
- A novel gene therapy for methamphetamine- induced cognitive disorder with a hyper-acidified fusion variant of DnaJB1.Molecular therapy. Nucleic acids · 2023Article
- Brain-derived neurotrophic factor protects serotonergic neurons against 3,4-methylenedioxymethamphetamine ("Ecstasy") induced cytoskeletal damage.Journal of neural transmission (Vienna, Austria : 1996) · 2022Article
- Autophagy Activator Drugs: A New Opportunity in Neuroprotection from Misfolded Protein Toxicity.International journal of molecular sciences · 2019Review
- Neuronal Cell Death and Degeneration through Increased Nitroxidative Stress and Tau Phosphorylation in HIV-1 Transgenic Rats.PloS one · 2017Article
- Adaptive Plasticity in the Hippocampus of Young Mice Intermittently Exposed to MDMA Could Be the Origin of Memory Deficits.Molecular neurobiology · 2016Article
- Hippocampal Wnt Signaling: Memory Regulation and Hormone Interactions.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016Review
- Caloric restriction mimetic 2-deoxyglucose maintains cytoarchitecture and reduces tau phosphorylation in primary culture of mouse hippocampal pyramidal neurons.In vitro cellular & developmental biology. Animal · 2015Article
- MDMA administration during adolescence exacerbates MPTP-induced cognitive impairment and neuroinflammation in the hippocampus and prefrontal cortex.Psychopharmacology · 2014Article
- Neuroprotective effects of lithium: implications for the treatment of Alzheimer's disease and related neurodegenerative disorders.ACS chemical neuroscience · 2014Review
- Detrimental effects of diet-induced obesity on τ pathology are independent of insulin resistance in τ transgenic mice.Diabetes · 2013Article
- Effects of Repeated Administration of 3,4-methylenedioxymethamphetamine (MDMA) on Avoidance Memory and Cell Density in Rats' Hippocampus.Basic and clinical neuroscience · 2013Article
- γ-Aminobutyric acid type A (GABAA) receptor activation modulates tau phosphorylation.The Journal of biological chemistry · 2012Article
- Induction of the Wnt antagonist Dickkopf-1 is involved in stress-induced hippocampal damage.PloS one · 2011Article
- The ugly side of amphetamines: short- and long-term toxicity of 3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy'), methamphetamine and D-amphetamine.Biological chemistry · 2011Review
- Molecular and cellular mechanisms of ecstasy-induced neurotoxicity: an overview.Molecular neurobiology · 2009Review
- Behavioral and Stereological Analysis of the Effects of Intermittent Feeding Diet on the Orally Administrated MDMA ("ecstasy") in Mice.Innovations in clinical neuroscienceArticle
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
3,4-Methylenedioxymethamphetamine (MDMA) ("Ecstasy") produces neurotoxic effects, which result into an impairment of learning and memory and other neurological dysfunctions. We examined whether MDMA induces increases in tau protein phosphorylation, which are typically associated with Alzheimer's disease and other chronic neurodegenerative disorders. We injected mice with MDMA at cumulative doses of 10-50 mg/kg intraperitoneally, which are approximately equivalent to doses generally consumed by humans. MDMA enhanced the formation of reactive oxygen species and induced reactive gliosis in the hippocampus, without histological evidence of neuronal loss. An acute or 6 d treatment with MDMA increased tau protein phosphorylation in the hippocampus, revealed by both anti-phospho(Ser(404))-tau and paired helical filament-1 antibodies. This increase was restricted to the CA2/CA3 subfields and lasted 1 and 7 d after acute and repeated MDMA treatment, respectively. Tau protein was phosphorylated as a result of two nonredundant mechanisms: (1) inhibition of the canonical Wnt (wingless-type MMTV integration site family) pathway, with ensuing activation of glycogen synthase kinase-3beta; and (2) activation of type-5 cyclin-dependent kinase (Cdk5). MDMA induced the expression of the Wnt antagonist, Dickkopf-1, and the expression of the Cdk5-activating protein, p25. In addition, the increase in tau phosphorylation was attenuated by strategies that rescued the Wnt pathway or inhibited Cdk5. Finally, an impairment in hippocampus-dependent spatial learning was induced by doses of MDMA that increased tau phosphorylation, although the impairment outlasted this biochemical event. We conclude that tau hyperphosphorylation in the hippocampus may contribute to the impairment of learning and memory associated with MDMA abuse.
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