Acta Scientific Gastrointestinal Disorders (ASGIS)(ISSN: 2582-1091)

Research Article Volume 5 Issue 3

Functional Foods for Cognitive Development and Memory in People with Down Syndrome

Adriana Budelon of Macedo*

Estácio de Sá University - São Paulo-SP, Brazil

*Corresponding Author: Adriana Budelon of Macedo, Estácio de Sá University - São Paulo-SP, Brazil.

Received: January 13, 2022; Published: February 22, 2022

Abstract

Down syndrome or trisomy of par 21 is a genetically determined human condition that promotes intellectual disability and functional changes interfering in development. Food can combat free radicals by attenuating brain aging in people with Down Syndrome. This article aimed to present information about functional foods that can contribute to cognitive improvement and brain development in people with Down Syndrome. There is evidence that foods that are sources of choline, phosphatadilcholine and phosphatadilserine, such as green tea and turmeric, through supplementation can contribute to brain function. This is due to the neuroprotective compounds present in turmeric and choline being the precursor of neurotransmitters.

Keywords: Trisomy; Alzheimer 'S; Green Tea

References

  1. 13 Guidelines for Attention to People with Down Syndrome.
  2. Roieski IM. “Evaluation of the usual diet of adolescents with down syndrome”. Revista Saúdecom2 (2010): 130-138.
  3. Prado MB., et al. “Nutritional follow-up of patients with Downsyndrome treated in a pediatric office”. World Health (1995) (2009): 335-346.
  4. ‌Scott JE. “Phosphatidylcholine Synthesis, Secretion, and Reutilization During Differentiation of the Surfactant-Producing Type II Alveolar Cell from Fetal Rabbit Lungs”. Experimental Lung Research4 (1992): 563-580.
  5. ‌Strupp BJ., et al. “Maternal choline supplementation: A potential prenatal treatment for Down syndrome and Alzheimer’s disease”. Current Alzheimer research 1 (2016): 97-106.
  6. ‌Siarey RJ., et al. “Altered signaling pathways underlying abnormal hippocampal synaptic plasticity in the Ts65Dn mouse model of Down syndrome”. Journal of Neurochemistry4 (2006): 1266-1277.
  7. ‌Coppus A., et al. “Dementia and mortality in persons with Down’s syndrome”. Journal of Intellectual Disability Research10 (2006): 768-777.
  8. ‌De la Torre R., et al. “Epigallocatechin-3-gallate, a DYRK1A inhibitor, rescues cognitive deficits in Down syndrome mouse models and in humans”. Molecular Nutrition and Food Research2 (2013): 278-288.
  9. ‌Zhang C., et al. “Curcumin Decreases Amyloid-β Peptide Levels by Attenuating the Maturation of Amyloid-β Precursor Protein”. Journal of Biological Chemistry37 (2010): 28472-28480.
  10. ‌Moon J., et al. “Perinatal choline supplementation improves cognitive functioning and emotion regulation in the Ts65Dn mouse model of Down syndrome”. Behavioral Neuroscience3 (2010): 346-361.
  11. ‌Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline”. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. PubMed. Washington (DC): National Academies Press (US) (1998).
  12. Cohn J., et al. “Dietary Phospholipids and Intestinal Cholesterol Absorption”. Nutrients2 (2010): 116-127.
  13. Karmiloff K and Karmiloff-Smith A. “Pathways to language: From fetus to adolescent”. Cambridge, MA: Harvard University Press (2002).
  14. Schwartzman JS. “Down syndrome”. São Paulo: Memnon (1999).
  15. Sheehan R., et al. “Dementia diagnostic criteria in Down syndrome”. International Journal of Geriatric Psychiatry8 (2014): 857-863.
  16. Alzheimer's disease: Pathophysiological and pharmacological aspects (2022).
  17. Pennington BF., et al. “The Neuropsychology of Down Syndrome Evidence for Hippocampal Dysfunction”. Child Development 74 (2003): 75-93.
  18. Roizen NJ and Patterson D. “Down’s syndrome”. The Lancet 9365 (2003): 1281-1289.
  19. Wisniewski KE., et al. “Occurrence of neuropathological changes and dementia of Alzheimer’s disease in Down’s syndrome”. Annals of Neurology3 (1985): 278-282.
  20. ‌Mann DM., et al. “The topography of plaques and tangles in Down’s syndrome patients of different ages”. Neuropathology and Applied Neurobiology5 (1986): 447-457.
  21. Cummings BJ., et al. “β-Amyloid Accumulation Correlates with Cognitive Dysfunction in the Aged Canine”. Neurobiology of Learning and Memory1 (1996): 11-23.
  22. ‌Tagarelli A., et al. “Alois Alzheimer: a hundred years after the discovery of the eponymous disorder”. International journal of biomedical science: IJBS2 (2006): 196-204.
  23. DSM-5 AMERICAN PSYCHIATRIC ASSOCIATION.
  24. Malamud N. “Neuropathology of Organic Brain Syndromes Associated with Aging”. Advances in Behavioral Biology (1972): 63-87.
  25. Wiseman FK., et al. “A genetic cause of Alzheimer disease: mechanistic insights from Down syndrome”. Nature Reviews Neuroscience9 (2015): 564-574.
  26. Griffiths-Jones S. “The microRNA Registry”. Nucleic Acids Research90001 (2004): 109D111.
  27. ‌Salehi A., et al. “Increased App expression in a mouse model of Down’s syndrome disrupts NGF transport and causes cholinergic neuron degeneration”. Neuron1 (2006): 29-42.
  28. ‌Sekar MC., et al. “Modulation of Epidermal Growth Factor stimulated ERK phosphorylation and cell motility by inositol trisphosphate kinase”. The FASEB JournalS1 (2010).
  29. Moreira LM., et al. “Down syndrome and its pathogenesis: considerations about genetic determinism”. Brazilian Journal of Psychiatry 22 (2000): 96-99.
  30. ‌Kleschevnikov AM., et al. “Deficits in Cognition and Synaptic Plasticity in a Mouse Model of Down Syndrome Ameliorated by GABAB Receptor Antagonists”. Journal of Neuroscience27 (2012): 9217-9227.
  31. Camargos EF de. “Randomized, double-blind, placebo-controlled trial on the use of trazodona in sleep disorders in patients with Alzheimer's disease”. Repositoriounbbr (2013).
  32. ‌Costa ACS., et al. “Behavioral validation of the Ts65Dn mouse model for Down syndrome of a genetic background free of the retinal degeneration mutation Pde6brd1”. Behavioural Brain Research1 (2010): 52-62.
  33. ‌Scott-McKean JJ and Costa ACS. “Exaggerated NMDA mediated LTD in a mouse model of Down syndrome and pharmacological rescuing by memantine”. Learning and Memory12 (2011): 774-778.
  34. Lima SC., et al. “Down syndrome: exploratory study of memory in the context of schooling”. Science and Cognition2 (2009): 35-46.
  35. ‌Mukhtar H and Ahmad N. “Tea polyphenols: prevention of cancer and optimizing health”. The American Journal of Clinical Nutrition6 (2000): 1698S1702S.
  36. González de Mejía E. “The chemoprotective effect of tea and its compounds”. Latin American Archives of Nutrition2 (2003): 111-118.
  37. ‌Cheng TO. “All teas are not created equal: The Chinese green tea and cardiovascular health”. International Journal of Cardiology3 (2006): 301-308.
  38. ‌Torre R de la., et al. “Safety and efficacy of cognitive training plus epigallocatechin-3-gallate in young adults with Down’s syndrome (TESDAD): a double-blind, randomised, placebo-controlled, phase 2 trial”. The Lancet Neurology8 (2016): 801-810.
  39. Da Mesquita S., et al. “Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease”. Nature7717 (2018): 185-191.
  40. ‌Noguchi-Shinohara M., et al. “Consumption of Green Tea, but Not Black Tea or Coffee, Is Associated with Reduced Risk of Cognitive Decline”. Bayer A, editor”. PLoS ONE5 (2014): e96013.
  41. Stringer M., et al. “Low dose EGCG treatment beginning in adolescence does not improve cognitive impairment in a Down syndrome mouse model”. Pharmacology, Biochemistry, and Behavior 138 (2015): 70-79.
  42. Souchet B., et al. “Pharmacological correction of excitation/inhibition imbalance in Down syndrome mouse models”. Frontiers in Behavioral Neuroscience 9 (2015): 267.
  43. ‌Guedj F., et al. “Green tea polyphenols rescue of brain defects induced by overexpression of DYRK1A”. PloS One2 (2009): e4606.
  44. Kulkarni S and Dhir A. “An overview of curcumin in neurological disorders”. Indian Journal of Pharmaceutical Sciences2 (2010): 149.
  45. ANTIOXIDANT POWER OF TURMON ON DEPRESSION - Brazil School. Monographs Brasil Escola (2022).
  46. ‌Xu Y., et al. “Curcumin prevents corticosterone-induced neurotoxicity and abnormalities of neuroplasticity via 5-HT receptor pathway”. Journal of Neurochemistry5 (2011): 784-795.
  47. ‌Ringman J., et al. “A Potential Role of the Curry Spice Curcumin in Alzheimers Disease”. Current Alzheimer Research2 (2005): 131-136.
  48. Aggarwal BB., et al. “Anticancer potential of curcumin: preclinical and clinical studies”. Anticancer Research1A (2003): 363-398.
  49. MINISTRY OF MONOGRAPH HEALTH OF THE SPECIES Curcuma longa (CURCUMA) Organization: Ministry of Health and Anvisa (2022).
  50. UNIVERSITY OF SÃO PAULO FACULTY OF PHARMACEUTICAL SCIENCES OF RIBEIRÃO PRETO (2022).
  51. Penry JT and Manore MM. “Choline: An Important Micronutrient for Maximal Endurance-Exercise Performance?” International Journal of Sport Nutrition and Exercise Metabolism2 (2008): 191-203.
  52. Zeisel SH., et al. “Concentrations of Choline-Containing Compounds and Betaine in Common Foods”. The Journal of Nutrition5 (2003): 1302-1307.
  53. Zeisel SH., et al. “Choline, an essential nutrient for humans”. FASEB Journal: official publication of the Federation of American Societies for Experimental Biology7 (1991): 2093-2098.
  54. ‌Zeisel SH. “Choline: an essential nutrient for humans”. Nutrition7-8 (2000): 669-671.
  55. Government of Canada SC. Search for Ingredients (2004).
  56. Yan J., et al. “Maternal choline supplementation programs greater activity of the phosphatidylethanolamine N-methyltransferase (PEMT) pathway in adult Ts65Dn trisomic mice”. FASEB Journal: official publication of the Federation of American Societies for Experimental Biology10 (2014): 4312-4323.
  57. Meck WH and Williams CL. “Choline supplementation during prenatal development reduces proactive interference in spatial memory”. Developmental Brain Research1-2 (1999): 51-59.
  58. ‌Ash JA., et al. “Maternal choline supplementation improves spatial mapping and increases basal forebrain cholinergic neuron number and size in aged Ts65Dn mice”. Neurobiology of Disease 70 (2014): 32-42.
  59. Kelley CM., et al. “Maternal choline supplementation differentially alters the basal forebrain cholinergic system of young-adult Ts65Dn and disomic mice”. Journal of Comparative Neurology6 (2014): 1390-410.
  60. Li Z and Vance DE. “Thematic Review Series: Glycerolipids.Phosphatidylcholine and choline homeostasis”. Journal of Lipid Research6 (2008): 1187-1194.
  61. Tait JF and Gibson D. “Measurement of membrane phospholipid asymmetry in normal and sickle-cell erythrocytes by means of annexin V binding”. The Journal of Laboratory and Clinical Medicine5 (1994): 741-748.
  62. ‌Akbar M., et al. “Docosahexaenoic acid: A positive modulator of Akt signaling in neuronal survival”. Proceedings of the National Academy of Sciences31 (2005): 10858-10863.
  63. Kim H-Y., et al. “Phosphatidylserine in the brain: Metabolism and function”. Progress in Lipid Research 56 (2014): 1-18.
  64. Moré MI., et al. “Positive Effects of Soy Lecithin-Derived Phosphatidylserine plus Phosphatidic Acid on Memory, Cognition, Daily Functioning, and Mood in Elderly Patients with Alzheimer’s Disease and Dementia”. Advances in Therapy12 (2014): 1247-1262.
  65. Salehi A., et al. “Increased App expression in a mouse model of Down’s syndrome disrupts NGF transport and causes cholinergic neuron degeneration”. Neuron1 (2006): 29-42.
  66. Cairney CJ., et al. “A systems biology approach to Down syndrome: Identification of Notch/Wnt dysregulation in a model of stem cells aging”. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease4 (2009): 353-363.
  67. Tlili A., et al. “DYRK1A overexpression decreases plasma lecithin:cholesterol acyltransferase activity and apolipoprotein A-I levels”. Molecular Genetics and Metabolism 110.3 (2013): 371-377.
  68. Effects of phosphatidylserine on different memory models [VHL]. pesquisa.bvsalud.org (2022).

Citation

Citation: Adriana Budelon of Macedo. “Functional Foods for Cognitive Development and Memory in People with Down Syndrome”. Acta Scientific Gastrointestinal Disorders 5.3 (2022): 51-58.

Copyright

Copyright: © 2022 Adriana Budelon of Macedo. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




Metrics

Acceptance rate35%
Acceptance to publication20-30 days

Indexed In




News and Events


  • Certification for Review
    Acta Scientific certifies the Editors/reviewers for their review done towards the assigned articles of the respective journals.
  • Submission Timeline for Upcoming Issue
    The last date for submission of articles for regular Issues is December 25, 2024.
  • Publication Certificate
    Authors will be issued a "Publication Certificate" as a mark of appreciation for publishing their work.
  • Best Article of the Issue
    The Editors will elect one Best Article after each issue release. The authors of this article will be provided with a certificate of "Best Article of the Issue"

Contact US