In a recent study performed with cultured fetal neurons from individuals with Down syndrome, it was demonstrated that reactive oxygen species contributed to apoptosis, a process where the cell programs itself to die (Busciglio and Yankerl995). Antioxidants prevented this degeneration of the Down syndrome neurons. These results suggest oxidative damage may play a role in the Down syndrome brain, yet must be interpreted with caution. The neurons were removed from the body and then the experiments conducted. The direct effect of free radicals and antioxidants in the body must now be investigated. This study will hopefully initiate further research to delineate the role of oxidative damage in the aging process and in degeneration of the brain, especially in Alzheimer's disease (Herman 1981; Mecocci et al 1994). This is particularly relevant as all individuals with Down syndrome over the age of 35 develop Alzheimer-like neuropathology and between 15-40% fully develop Alzheimer's disease (Wisniewski and Rabe 1985; Kolata 1985; Rabe et al 1990).
Monocarbon metabolism is vital for a variety of biochemical processes (Rawn 1989). Some of the compounds whose synthesis is dependent on one-carbon metabolism include: adrenaline, choline (as in acetylcholine, a neurotransmitter and as in phosphatidylcholine, an essential component of cellular membranes) and components of RNA and DNA. Monocarbon metabolism involves the transfer of one-carbon units on carriers, which as their name implies, carry the one carbon units to other compounds. One carbon units are derived from common dietary components, serine, glycine, methionine and choline. Carriers for monocarbons include: THFA (tetrahydrofolic acid from the vitamin folate); S-adenosylmethionine(derived from the essential amino acid methionine); and enzyme-bound vitamin B12 (Rawn 1989). Dietary deficiency of these components can give rise to disorders of one carbon metabolism. So important is monocarbon metabolism to the cell that certain antibiotics and anti-cancer agents target this process. Dr. Lejeune, Dr. Peeters and their colleagues identified several defects in monocarbon metabolism in people with Down syndrome (Chadefaux et al 1985; Lejeune 1992; Peeters et al 1995; M.A. Peeters, personal communication). This research was conducted through the analysis of urine and plasma amino acids, experiments with supplemental folate and methionine, and analysis of drug sensitivities.
As described above, advances are being made in the area of nutrition and Down syndrome, particularly in the areas of monocarbon metabolism and cellular oxidation. Additional research is required to fully comprehend the role of nutrients and their potential benefit to people with Down syndrome.
Any nutritional program should be conducted under the supervision of a family physician.
(published with permission in writing from:http://www.dsrf.co.uk/)
