Green tea extracts containing epigallocatechin-3-gallate modulate facial development in Down syndrome

Starbuck, John M.; Llambrich, Sergi; González, Rubén; Albaigès, Julia; Sarlé, Anna; Wouters, Jens; González, Alejandro; Sevillano, Xavier; Sharpe, James; Torre, Rafael de la; Dierssen, Mara; Velde, Greetje Vande; Martínez‐Abadías, Neus

doi:10.1038/s41598-021-83757-1

Cited by 26 publications

(43 citation statements)

References 48 publications

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“…Changes in other domains have been investigated. Facial dysmorphology was improved in DS mouse models and also observed in young children treated with GTE-EGCG [230,232]. Nevertheless, Stringer et al [215] stressed the negative effect on long bones development in treated mice.…”

Section: Discussionmentioning

confidence: 99%

Dyrk1a from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome

Atas-Ozcan

Brault

Duchon

et al. 2021

Genes

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Down syndrome is the main cause of intellectual disabilities with a large set of comorbidities from developmental origins but also that appeared across life span. Investigation of the genetic overdosage found in Down syndrome, due to the trisomy of human chromosome 21, has pointed to one main driver gene, the Dual-specificity tyrosine-regulated kinase 1A (Dyrk1a). Dyrk1a is a murine homolog of the drosophila minibrain gene. It has been found to be involved in many biological processes during development and in adulthood. Further analysis showed its haploinsufficiency in mental retardation disease 7 and its involvement in Alzheimer’s disease. DYRK1A plays a role in major developmental steps of brain development, controlling the proliferation of neural progenitors, the migration of neurons, their dendritogenesis and the function of the synapse. Several strategies targeting the overdosage of DYRK1A in DS with specific kinase inhibitors have showed promising evidence that DS cognitive conditions can be alleviated. Nevertheless, providing conditions for proper temporal treatment and to tackle the neurodevelopmental and the neurodegenerative aspects of DS across life span is still an open question.

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Section: Discussionmentioning

confidence: 99%

Dyrk1a from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome

Atas-Ozcan

Brault

Duchon

et al. 2021

Genes

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“…Another recent trial showed that EGCG modulates facial development with dose-dependent effect if administered at low doses (30 mg/kg/day) before the age of three. Higher doses (100 mg/kg/day) would potentially have detrimental effects [107].…”

Section: Effects Of Catechins On Down Syndrome (Ds) Neurocognitive Disordersmentioning

confidence: 99%

Therapeutic Effects of Catechins in Less Common Neurological and Neurodegenerative Disorders

et al. 2021

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In recent years, neurological and neurodegenerative disorders research has focused on altered molecular mechanisms in search of potential pharmacological targets, e.g., imbalances in mechanisms of response to oxidative stress, inflammation, apoptosis, autophagy, proliferation, differentiation, migration, and neuronal plasticity, which occur in less common neurological and neurodegenerative pathologies (Huntington disease, multiple sclerosis, fetal alcohol spectrum disorders, and Down syndrome). Here, we assess the effects of different catechins (particularly of epigalocatechin-3-gallate, EGCG) on these disorders, as well as their use in attenuating age-related cognitive decline in healthy individuals. Antioxidant and free radical scavenging properties of EGCG -due to their phenolic hydroxyl groups-, as well as its immunomodulatory, neuritogenic, and autophagic characteristics, makes this catechin a promising tool against neuroinflammation and microglia activation, common in these pathologies. Although EGCG promotes the inhibition of protein aggregation in experimental Huntington disease studies and improves the clinical severity in multiple sclerosis in animal models, its efficacy in humans remains controversial. EGCG may normalize DYRK1A (involved in neural plasticity) overproduction in Down syndrome, improving behavioral and neural phenotypes. In neurological pathologies caused by environmental agents, such as FASD, EGCG enhances antioxidant defense and regulates placental angiogenesis and neurodevelopmental processes. As demonstrated in animal models, catechins attenuate age-related cognitive decline, which results in improvements in long-term outcomes and working memory, reduction of hippocampal neuroinflammation, and enhancement of neuronal plasticity; however, further studies are needed. Catechins are valuable compounds for treating and preventing certain neurodegenerative and neurological diseases of genetic and environmental origin. However, the use of different doses of green tea extracts and EGCG makes it difficult to reach consistent conclusions for different populations.

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“…A recent cross-sectional study of Starbuck et al (2021) investigated if green tea extracts with EGCG could modulate facial dysmorphologies DS [110]. These facial dysmorphologies can impair vital functions such as hearing, breathing, mastication, and health.…”

Section: Egcg In Relation To Cognitive Functioning Facial Shape and Body Weightmentioning

confidence: 99%

Dietary supplements for children with Down syndrome: exploration of current use and scientific evidence : Fieldwork and literature study

Haar¹,

Zeinstra²

2021

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Green tea extracts containing epigallocatechin-3-gallate modulate facial development in Down syndrome

Cited by 26 publications

References 48 publications

Dyrk1a from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome

Dyrk1a from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome

Therapeutic Effects of Catechins in Less Common Neurological and Neurodegenerative Disorders

Dietary supplements for children with Down syndrome: exploration of current use and scientific evidence : Fieldwork and literature study

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