ArticleScientific reports2019
Prenatal treatment with EGCG enriched green tea extract rescues GAD67 related developmental and cognitive defects in Down syndrome mouse models.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 53 citations in OpenAlex.
- Fasudil induces anti-inflammatory transcriptomic changes and increased proliferation in human trisomy 21 neural progenitor cells.Biology open · 2026Article
- Duplication-based genetic dissection of the Down syndrome critical region reveals its complex functional organization.G3 (Bethesda, Md.) · 2026Article
- Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions.Antioxidants (Basel, Switzerland) · 2026Review
- Anti-inflammatory and pro-proliferative effects of fasudil in human trisomy 21 neural progenitor cells.bioRxiv : the preprint server for biology · 2026Article
- The effect of maternal polyphenol intake on foetal neurodevelopment in rodent models: a narrative review.Journal of nutritional science · 2026Review
- Cardiopulmonary and Immune Alterations in the Ts65Dn Mouse Model of Down Syndrome and Modulation by Epigallocatechin-3-Gallate-Enriched Green Tea Extract.Pharmaceutics · 2025Article
- The role of Goldilocks protein kinase DYRK1A in embryonic development.Developmental biology · 2025Review
- Genetic knockdown of DYRK1A attenuates cognitive impairment, Aβ pathology, tauopathy and neuroinflammatory responses in mouse models of AD.Frontiers in immunology · 2025Article
- Sex-specific trisomic Dyrk1a-related skeletal phenotypes during development in a Down syndrome model.Disease models & mechanisms · 2024Article
- Sex specific emergence of trisomicbioRxiv : the preprint server for biology · 2024Article
- Prenatal treatment with preimplantation factor improves early postnatal neurogenesis and cognitive impairments in a mouse model of Down syndrome.Cellular and molecular life sciences : CMLS · 2024Article
- Article
- Understanding the genetic mechanisms and cognitive impairments in Down syndrome: towards a holistic approach.Journal of neurology · 2024Review
- Dissecting the contribution of human chromosome 21 syntenic regions to recognition memory processes in adult and aged mouse models of Down syndrome.Frontiers in behavioral neuroscience · 2024Article
- Identifying foetal forebrain interneurons as a target for monogenic autism risk factors and the polygenic 16p11.2 microdeletion.BMC neuroscience · 2023Article
- Green Tea Catechins Modulate Skeletal Development with Effects Dependent on Dose, Time, and Structure in a down Syndrome Mouse Model.Nutrients · 2022Article
- Catechins as a Potential Dietary Supplementation in Prevention of Comorbidities Linked with Down Syndrome.Nutrients · 2022Review
- The Challenging Pathway of Treatment for Neurogenesis Impairment in Down Syndrome: Achievements and Perspectives.Frontiers in cellular neuroscience · 2022Review
- MultimodalFrontiers in medicine · 2022Article
- Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down syndrome is a common genetic disorder caused by trisomy of chromosome 21. Brain development in affected foetuses might be improved through prenatal treatment. One potential target is DYRK1A, a multifunctional kinase encoded by chromosome 21 that, when overexpressed, alters neuronal excitation-inhibition balance and increases GAD67 interneuron density. We used a green tea extract enriched in EGCG to inhibit DYRK1A function only during gestation of transgenic mice overexpressing Dyrk1a (mBACtgDyrk1a). Adult mice treated prenatally displayed reduced levels of inhibitory markers, restored VGAT1/VGLUT1 balance, and rescued density of GAD67 interneurons. Similar results for gabaergic and glutamatergic markers and interneuron density were obtained in Dp(16)1Yey mice, trisomic for 140 chromosome 21 orthologs; thus, prenatal EGCG exhibits efficacy in a more complex DS model. Finally, cognitive and behaviour testing showed that adult Dp(16)1Yey mice treated prenatally had improved novel object recognition memory but do not show improvement with Y maze paradigm. These findings provide empirical support for a prenatal intervention that targets specific neural circuitries.
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