Plant Compound Apigenin Reduces Cognitive Deficits in Mouse Model of Down Syndrome

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Child Downs Syndrome

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Mice treated with apigenin had much better memory and developmental turning point ratings.

The plant substance apigenin enhanced the cognitive and memory deficits normally seen in a mouse design of Down syndrome, according to a research study by scientists at the National Institutes of Health and other organizations.

Apigenin is discovered in chamomile flowers, parsley, celery, peppermint, and citrus fruits. The scientists fed the substance to pregnant mice bring fetuses with Down syndrome qualities and after that to the animals after they were born and as they developed.

The findings raise the possibility that a treatment to reduce the cognitive deficits seen in Down syndrome might one day be provided to pregnant ladies whose fetuses have actually been detected with Down syndrome through prenatal screening. The research study appears in the American Journal of Human Genetics.

Down syndrome is a set of signs arising from an additional copy or piece of chromosome 21. The intellectual and developmental specials needs accompanying the condition are thought to arise from reduced brain development triggered by increased swelling in the fetal brain.

Apigenin is not understood to have any poisonous results, and previous research studies have actually shown that it is an anti-oxidant that decreases swelling. Unlike numerous substances, it is soaked up through the placenta and the blood brain barrier, the cellular layer that avoids possibly damaging compounds from getting in the brain.

Compared to mice with Down signs whose moms were not fed apigenin, those exposed to the substance revealed enhancements in tests of developmental turning points and had enhancements in spatial and olfactory memory. Tests of gene activity and protein levels revealed the apigenin-treated mice had less swelling and increased capillary and nerve system development.

Reference: “Apigenin as a Candidate Prenatal Treatment for Trisomy 21: Effects in Human Amniocytes and the Ts1Cje Mouse Model” by Faycal Guedj, Ashley E. Siegel, Jeroen L.A. Pennings, Fatimah Alsebaa, Lauren J. Massingham, Umadevi Tantravahi and Diana W. Bianchi, 23 October 2020, American Journal of Human Genetics.
DOI: 10.1016/j.ajhg.2020.10.001

The NIH part of the research study was performed at the National Human Genome Research Institute (NHGRI). Additional financing was supplied by the NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).



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