By Christina Bolander-Gouaille
Over the past 15 years the learn on homocysteine and the supplements fascinated about its metabolism has develop into very dynamic. approximately 1,500 courses at the topic at the moment are released every year. The examine has lengthy customarily fascinated by the organization among homocysteine and heart problems, but in addition being pregnant issues/ fetal malformations. there's, notwithstanding, an expanding curiosity within the connection among the homocysteine metabolism and neuropsychiatric disorder with a steeply expanding variety of courses. particularly, the organization among homocysteine metabolism and cognitive decline/dementia draws a lot curiosity. If basic, non-toxic homocysteine-lowering therapy with supplements can decrease the prevalence of, or hold up the onset of dementia, it'll have a big impression in societies with a speedily expanding variety of aged in danger for dementia. This booklet summarises the learn in the neuropsychiatric box, but in addition supplies an outline of the underlying biochemistry and of diagnostic elements. approximately 1,000 references are given. Christina Bolander-Gouaille, a pharmacist, has for over 10 years specialized in writing reviews/monographs on homocysteine and comparable supplements. this can be her 3rd ebook in a chain edited by way of Springer Verlag. This booklet, despite the fact that, is written in collaboration with Teodoro Bottiglieri, who's director of neuropharmacology and senior examine scientist at Baylor collage, Institute for Metabolic illnesses in Dallas, united states.
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Extra resources for Homocysteine Related Vitamins and Neuropsychiatric Disorders
Other proposed mechanisms There is evidence that Hcy is converted to Hcy thiolactone by methionyltRNA synthetase in cultured mammalian cells (Jakubowski H and Goldman E, 1993, Jakubowski H, 1997). , 2000a). In cultured human cells and human serum Hcy thiolactone reacts with proteins by a mechanism involving homocysteinylation of protein lysine residues. g. Hcy-induced vascular damage. This pathway was found to be dominant when MS and/or CBS are inactive, either because of mutations, and/or because of deficiencies of folate, vitamin B6, or vitamin B12 (Jakubowski H, 1997, 1999 and 2000b).
The presence of this H475Y variant, found in 6 out of 75 subjects, was associated with lower folate and higher tHcy levels in a Caucasian population. , 2000). Folate transport into the cell is mediated by a membrane-bound protein (FR-α) with a high binding affinity for 5-methyl-THF, and by the reduced folate carrier (RFC). , 2000c). The prevalence of homozygosity in different populations is about 25-30%. , 2001). How can Homocysteine be Neurotoxic ? The proposed pathogenetic mechanisms, by which hyperhomocysteinemia may cause vascular damage, cognitive impairment, psychiatric and neurological complications, congenital defects, and pregnancy complications, converge.
2000). Neural membrane aminophospholipids contain very high concentrations of docosahexaenoic acid, which suggests a major role in the function of the CNS (Burdge G, 1998). , 2000). , 1999). Recent data from a study of human umbilical endothelial cells suggest that vitamin B6 had a protective effect by enhancing the production of prostacyclin, thereby reducing cell injury (Chang SJ, 1999). Other proposed mechanisms There is evidence that Hcy is converted to Hcy thiolactone by methionyltRNA synthetase in cultured mammalian cells (Jakubowski H and Goldman E, 1993, Jakubowski H, 1997).