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56. Cerebral folate deficiency with developmental delay, autism, and response to folinic acid

Author

Moretti, P., primary, Sahoo, T., additional, Hyland, K., additional, Bottiglieri, T., additional, Peters, S., additional, del Gaudio, D., additional, Roa, B., additional, Curry, S., additional, Zhu, H., additional, Finnell, R. H., additional, Neul, J. L., additional, Ramaekers, V. T., additional, Blau, N., additional, Bacino, C. A., additional, Miller, G., additional, and Scaglia, F., additional

Published
2005
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61. Genetic Predisposition to Neural Tube Defects?

Author

Bottiglieri T and Gibson Km

Subjects
Genetics, medicine.anatomical_structure, Methylenetetrahydrofolate reductase (NADPH), Polymorphism (computer science), Pediatrics, Perinatology and Child Health, Neural tube, medicine, Genetic predisposition, Biology, Risk factor, Genetic determinism
Published
2000
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75. High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial.

Author

Aisen PS, Schneider LS, Sano M, Diaz-Arrastia R, van Dyck CH, Weiner MF, Bottiglieri T, Jin S, Stokes KT, Thomas RG, Thal LJ, Alzheimer Disease Cooperative Study, Aisen, Paul S, Schneider, Lon S, Sano, Mary, Diaz-Arrastia, Ramon, van Dyck, Christopher H, Weiner, Myron F, Bottiglieri, Teodoro, and Jin, Shelia

Abstract

Context: Blood levels of homocysteine may be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophysiology by vascular and direct neurotoxic mechanisms. Even in the absence of vitamin deficiency, homocysteine levels can be reduced by administration of high-dose supplements of folic acid and vitamins B(6) and B(12). Prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline.Objective: To determine the efficacy and safety of B vitamin supplementation in the treatment of AD.Design, Setting, and Patients: A multicenter, randomized, double-blind controlled clinical trial of high-dose folate, vitamin B(6), and vitamin B(12) supplementation in 409 (of 601 screened) individuals with mild to moderate AD (Mini-Mental State Examination scores between 14 and 26, inclusive) and normal folic acid, vitamin B(12), and homocysteine levels. The study was conducted between February 20, 2003, and December 15, 2006, at clinical research sites of the Alzheimer Disease Cooperative Study located throughout the United States.Intervention: Participants were randomly assigned to 2 groups of unequal size to increase enrollment (60% treated with high-dose supplements [5 mg/d of folate, 25 mg/d of vitamin B(6), 1 mg/d of vitamin B(12)] and 40% treated with identical placebo); duration of treatment was 18 months.Main Outcome Measure: Change in the cognitive subscale of the Alzheimer Disease Assessment Scale (ADAS-cog).Results: A total of 340 participants (202 in active treatment group and 138 in placebo group) completed the trial while taking study medication. Although the vitamin supplement regimen was effective in reducing homocysteine levels (mean [SD], -2.42 [3.35] in active treatment group vs -0.86 [2.59] in placebo group; P < .001), it had no beneficial effect on the primary cognitive measure, rate of change in ADAS-cog score during 18 months (0.372 points per month for placebo group vs 0.401 points per month for active treatment group, P = .52; 95% confidence interval of rate difference, -0.06 to 0.12; based on the intention-to-treat generalized estimating equations model), or on any secondary measures. A higher quantity of adverse events involving depression was observed in the group treated with vitamin supplements.Conclusion: This regimen of high-dose B vitamin supplements does not slow cognitive decline in individuals with mild to moderate AD.Trial Registration: clinicaltrials.gov Identifier: NCT00056225. [ABSTRACT FROM AUTHOR]

Published
2008
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88. The switch mechanism and the bipolar/unipolar dichotomy.

Author

Carney, M. W. P., Chary, T. K. N., Bottiglieri, T., Reynolds, E. H., Carney, M W, and Chary, T K

Subjects
METHIONINE, CLINICAL trials, PLACEBOS, BIPOLAR disorder, HYPOMANIA, CEREBROSPINAL fluid, ADENOSYLMETHIONINE, COMPARATIVE studies, EMOTIONS, INTRAVENOUS injections, RESEARCH methodology, MEDICAL cooperation, ORAL drug administration, RESEARCH, EVALUATION research, RANDOMIZED controlled trials, THERAPEUTICS, PSYCHOLOGY
Abstract

During open trials of intravenous and oral S-adenosyl methionine (SAM) and a placebo-controlled trial of intravenous SAM in 29 patients, 25 patients had SAM and four had placebo (27 courses of SAM, two of the patients receiving two trials a piece). Nine of 11 bipolar patients (all SAM-treated) switched into elevated mood state (hypomania, mania and euphoria) and two did not respond. Six endogenous unipolar patients improved and five did not. No non-endogenous patient or placebo patient responded for more than 14 days. No unipolar patient switched into elated mood. In eleven (38%) trials and nine (33%) patients there was a switch from depression to elation. Biochemical data from the cerebrospinal fluid of eight patients suggested that the role of the dopaminergic system should be further explored. [ABSTRACT FROM AUTHOR]

Published
1989
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91. Association of homocysteine with plasma amyloid protein in aging and neurodegenerative disease

Author

Irizarry, M C., Gurol, M E., Raju, S, Diaz-Arrastia, R, Locascio, J J., Tennis, M, Hyman, B T., Growdon, J H., Greenberg, S M., and Bottiglieri, T

Abstract

Elevated plasma total homocysteine (tHcy) is a risk factor for cardiovascular disease and is reported to be an independent risk factor for Alzheimer disease (AD) and cognitive decline. tHcy may potentiate neurotoxic and vasculopathic processes, including amyloid protein (A) metabolism, implicated in neurodegenerative diseases.

Published
2005
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94. Subacute Combined Degeneration With High Serum Vitamin B12 Level and Abnormal Vitamin B12 Binding Protein: New Cause of an Old Syndrome

Author

Reynolds, E. H., Bottiglieri, T., Laundy, M., Stern, J., Payan, J., Linnell, J., and Faludy, J.

Abstract

• Subacute combined degeneration of the spinal cord due to vitamin B12 deficiency invariably has been associated with a low serum vitamin B12 level. We describe a young man who presented with a unique syndrome of subacute combined degeneration associated with high serum vitamin B12 level, low red blood cell vitamin B12 level, and an abnormal plasma vitamin B12-binding protein. Uptake of cobalamin by his leukocytes in vitro was inhibited by his own but not by normal control plasma. Intensive hydroxocobalamin (vitamin B12) treatment was associated with clinical and electrophysiologic recovery accompanied by normalization of mean corpuscular volume, red blood cell vitamin B12 level, plasma homocysteine, and urinary methylmalonic acid. The subacute combined degeneration was probably precipitated by treatment with folic acid as the significance of his high serum vitamin B12 level was not apparent when he first presented with megaloblastic anemia 3 years earlier. To our knowledge, this is the first example of neurologic disease associated with high serum vitamin B12 level and provides further evidence that sometimes a serum vitamin B12 level may not be a reliable guide to vitamin B12 deficiency.

Published
1993
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95. Demyelination and decreased Sadenosylmethionine in 510methylenetetrahydrofolate reductase deficiency

Author

Hyland, K., Smith, I., Bottiglieri, T., Perry, J., Wendel, U., Clayton, P. T., and Leonard, J. V.

Abstract

We previously described demyelination in the brain and subacute combined degeneration of the spinal cord in a patient with 5,10-methylenetetrahydrofolate reductase deficiency. To assess the role of methionine, S-adenosylmethionine, folate, and neurotransmitter amine metabolism in the demyelination process, we measured these metabolites in CSF from this patient; the findings are compared with those obtained from three patients in whom neurologic deterioration had been halted by the administration of betaine. Folate concentrations were low, and amine and biopterin metabolism were abnormal in all patients. Methionine and S-adenosylmethionine concentrations were undetectable in the first patient. In those receiving betaine, methionine concentrations were proportional to the dose administered and S-adenosylmethionine concentrations were near normal. The results provide the first evidence for an association between defective S-adenosylmethionine metabolism and demyelination in humans.

Published
1988

96. One-carbon metabolism nutrient status and plasma s-adenosylmethionine concentrations in middle-aged and older Chinese in Singapore

Author

Inoue-Choi, M., Nelson, H. H., Kim Robien, Arning, E., Bottiglieri, T., Koh, W. -P, and Yuan, J. -M

Subjects
Original Article
Abstract

S-adenosylmethionine (SAM) is a primary methyl donor for the methylation of many molecules including DNA. DNA methylation is believed to play an important role in functions of cells and genes. Dietary, genetic and metabolic factors that influence systematic SAM levels are not fully understood. We conducted cross-sectional analysis to evaluate associations between plasma concentrations of one-carbon metabolism nutrients and metabolites and plasma SAM concentrations using healthy individuals within the Singapore Chinese Health Study. Plasma SAM, betaine, choline, folate, total homocysteine (Hcy), methionine, S-adenosylhomocysteine (SAH), vitamin B(6) and vitamin B(12) concentrations were quantified. Genotypes of methionine adenosyltransferases (MAT1A, MAT2A and MAT2B) were also determined. Linear regression and path analysis were performed to depict the directed dependencies in one-carbon metabolism. Age and body mass index were positively associated while cigarette smoking were inversely associated with plasma SAM concentrations. Plasma choline, methionine and SAH were positively and strongly associated with plasma SAM after adjustment for confounders. Plasma betaine and folate were positively associated with plasma SAM only in men. Men carrying the variant MAT1A genotypes had lower plasma SAM concentrations than men carrying the wild type genotype (p for gene x gender interaction = 0.02). This effect modification by gender was restricted to individuals with low plasma methionine. In conclusion, plasma choline, methionine and SAH were strongly associated with plasma SAM concentrations. The MAT1A genetic polymorphism may impact plasma SAM concentrations in men with low plasma methionine concentrations.

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