ORIGINAL ARTICLESFolic Acid and B12 in Autism and Neuropsychiatric Disturbances of Childhood
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Cited by (20)
Increased homocysteine levels correlate with the communication deficit in children with autism spectrum disorder
2015, Psychiatry ResearchCitation Excerpt :The regulation of homocysteine concentration depends on several metabolic routes and enzymes and depends on availability of some form of folate and vitamin B12. A recent study performed in Omani children with ASD found a decreased vitamin B12 and folate concentration (Al-Farsi et al., 2013) however no significant alterations have been found in other studies (Adams et al., 2011; Lowe et al., 1981;Melnyk et al., 2012). Conversely, the expression of some of the vitamin B12- or folate-dependent enzymes involved in homocysteine metabolic routes has been shown to be altered in patients with ASD (Frustaci et al., 2012 for review).
Low folate and vitamin B12 nourishment is common in Omani children with newly diagnosed autism
2013, NutritionCitation Excerpt :There is evidence that the variation in levels of two important nutrients, folate and vitamin B12 [14–16], is strongly relevant for ASD. These two nutrients have been suggested to play a vital role in cognitive functions [17] similar to those often found to be disturbed in children with ASDs [14,18–20]. Building on these emerging data showing that Arab populations tend to have folate and vitamin B12 deficiencies, we initially conducted a preliminary study on screening the folate and vitamin B12 status and we reported that a low status of these two vitamins was associated with hyperhomocysteinemia in Omani autistic children [21].
Folate and methionine metabolism in autism: A systematic review
2010, American Journal of Clinical NutritionFolate and homocysteine metabolism in neural plasticity and neurodegenerative disorders
2003, Trends in NeurosciencesFolic acid in neurodevelopment and child psychiatry
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This investigation was supported in part by National Research Service Award MH 07704–02, CCRC grant #RR 00125, MH-CRC grant MH30929, Mr. Leonard Berger, the Baker Foundation, and the Ford Foundation.