On the etiopathogenesis and therapy of Down syndrome.

Abstract

The etiopathogenesis of Down syndrome is reviewed concentrating on the possible consequences of over-expression of cytoplasmic superoxide dismutase gene located in chromosome 21. Increased superoxide dismutase activity may generate free radical stress through overproduction of hydrogen peroxide. The significance of inadequate adaptive responses, i.e. increase of the selenoenzyme glutathione peroxidase activity in the central nervous system and in the thyroid gland is discussed. Suggestions are made for prevention of the progress of Down syndrome and intervention studies with antioxidant supplementation are proposed.

• Authors: E Antila, T Westermarck
• Journal: The International journal of developmental biology (Int J Dev Biol) Vol. 33 Issue 1 Pg. 183-8 (Mar 1989) ISSN: 0214-6282 [Print] Spain
• PMID: 2534992 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Antioxidants
• Free Radicals
• Superoxide Dismutase

Topics

• Antioxidants (therapeutic use)
• Cytoplasm (enzymology)
• Down Syndrome (etiology, genetics, therapy)
• Free Radicals
• Humans
• Superoxide Dismutase (biosynthesis, genetics)