Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial
Background Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine‐lowering treatment with B vitamins slows the rate of brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B vitamins on cognitive and...
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| Vydáno v: | International journal of geriatric psychiatry Ročník 27; číslo 6; s. 592 - 600 |
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| Hlavní autoři: | , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
Chichester, UK
John Wiley & Sons, Ltd
01.06.2012
Psychology Press Wiley Subscription Services, Inc |
| Témata: | |
| ISSN: | 0885-6230, 1099-1166, 1099-1166 |
| On-line přístup: | Získat plný text |
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| Abstract | Background
Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine‐lowering treatment with B vitamins slows the rate of brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B vitamins on cognitive and clinical decline (secondary outcomes) in the same study.
Methods
This was a double‐blind, single‐centre study, which included participants with MCI, aged ≥70 y, randomly assigned to receive a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B12 and 20 mg vitamin B6 (133 participants) or placebo (133 participants) for 2 y. Changes in cognitive or clinical function were analysed by generalized linear models or mixed‐effects models.
Results
The mean plasma total homocysteine was 30% lower in those treated with B vitamins relative to placebo. B vitamins stabilized executive function (CLOX) relative to placebo (P = 0.015). There was significant benefit of B‐vitamin treatment among participants with baseline homocysteine above the median (11.3 µmol/L) in global cognition (Mini Mental State Examination, P < 0.001), episodic memory (Hopkins Verbal Learning Test–delayed recall, P = 0.001) and semantic memory (category fluency, P = 0.037). Clinical benefit occurred in the B‐vitamin group for those in the upper quartile of homocysteine at baseline in global clinical dementia rating score (P = 0.02) and IQCODE score (P = 0.01).
Conclusion
In this small intervention trial, B vitamins appear to slow cognitive and clinical decline in people with MCI, in particular in those with elevated homocysteine. Further trials are needed to see if this treatment will slow or prevent conversion from MCI to dementia. Copyright © 2011 John Wiley & Sons, Ltd. |
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| AbstractList | Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine-lowering treatment with B vitamins slows the rate of brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B vitamins on cognitive and clinical decline (secondary outcomes) in the same study.BACKGROUNDHomocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine-lowering treatment with B vitamins slows the rate of brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B vitamins on cognitive and clinical decline (secondary outcomes) in the same study.This was a double-blind, single-centre study, which included participants with MCI, aged ≥ 70 y, randomly assigned to receive a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B(12) and 20 mg vitamin B(6) (133 participants) or placebo (133 participants) for 2 y. Changes in cognitive or clinical function were analysed by generalized linear models or mixed-effects models.METHODSThis was a double-blind, single-centre study, which included participants with MCI, aged ≥ 70 y, randomly assigned to receive a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B(12) and 20 mg vitamin B(6) (133 participants) or placebo (133 participants) for 2 y. Changes in cognitive or clinical function were analysed by generalized linear models or mixed-effects models.The mean plasma total homocysteine was 30% lower in those treated with B vitamins relative to placebo. B vitamins stabilized executive function (CLOX) relative to placebo (P = 0.015). There was significant benefit of B-vitamin treatment among participants with baseline homocysteine above the median (11.3 µmol/L) in global cognition (Mini Mental State Examination, P < 0.001), episodic memory (Hopkins Verbal Learning Test-delayed recall, P = 0.001) and semantic memory (category fluency, P = 0.037). Clinical benefit occurred in the B-vitamin group for those in the upper quartile of homocysteine at baseline in global clinical dementia rating score (P = 0.02) and IQCODE score (P = 0.01).RESULTSThe mean plasma total homocysteine was 30% lower in those treated with B vitamins relative to placebo. B vitamins stabilized executive function (CLOX) relative to placebo (P = 0.015). There was significant benefit of B-vitamin treatment among participants with baseline homocysteine above the median (11.3 µmol/L) in global cognition (Mini Mental State Examination, P < 0.001), episodic memory (Hopkins Verbal Learning Test-delayed recall, P = 0.001) and semantic memory (category fluency, P = 0.037). Clinical benefit occurred in the B-vitamin group for those in the upper quartile of homocysteine at baseline in global clinical dementia rating score (P = 0.02) and IQCODE score (P = 0.01).In this small intervention trial, B vitamins appear to slow cognitive and clinical decline in people with MCI, in particular in those with elevated homocysteine. Further trials are needed to see if this treatment will slow or prevent conversion from MCI to dementia.CONCLUSIONIn this small intervention trial, B vitamins appear to slow cognitive and clinical decline in people with MCI, in particular in those with elevated homocysteine. Further trials are needed to see if this treatment will slow or prevent conversion from MCI to dementia. Background Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine‐lowering treatment with B vitamins slows the rate of brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B vitamins on cognitive and clinical decline (secondary outcomes) in the same study. Methods This was a double‐blind, single‐centre study, which included participants with MCI, aged ≥70 y, randomly assigned to receive a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B12 and 20 mg vitamin B6 (133 participants) or placebo (133 participants) for 2 y. Changes in cognitive or clinical function were analysed by generalized linear models or mixed‐effects models. Results The mean plasma total homocysteine was 30% lower in those treated with B vitamins relative to placebo. B vitamins stabilized executive function (CLOX) relative to placebo (P = 0.015). There was significant benefit of B‐vitamin treatment among participants with baseline homocysteine above the median (11.3 µmol/L) in global cognition (Mini Mental State Examination, P < 0.001), episodic memory (Hopkins Verbal Learning Test–delayed recall, P = 0.001) and semantic memory (category fluency, P = 0.037). Clinical benefit occurred in the B‐vitamin group for those in the upper quartile of homocysteine at baseline in global clinical dementia rating score (P = 0.02) and IQCODE score (P = 0.01). Conclusion In this small intervention trial, B vitamins appear to slow cognitive and clinical decline in people with MCI, in particular in those with elevated homocysteine. Further trials are needed to see if this treatment will slow or prevent conversion from MCI to dementia. Copyright © 2011 John Wiley & Sons, Ltd. Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine-lowering treatment with B vitamins slows the rate of brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B vitamins on cognitive and clinical decline (secondary outcomes) in the same study. This was a double-blind, single-centre study, which included participants with MCI, aged ≥70 y, randomly assigned to receive a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B12 and 20 mg vitamin B6 (133 participants) or placebo (133 participants) for 2 y. Changes in cognitive or clinical function were analysed by generalized linear models or mixed-effects models. The mean plasma total homocysteine was 30% lower in those treated with B vitamins relative to placebo. B vitamins stabilized executive function (CLOX) relative to placebo (P = 0.015). There was significant benefit of B-vitamin treatment among participants with baseline homocysteine above the median (11.3 ...mol/L) in global cognition (Mini Mental State Examination, P < 0.001), episodic memory (Hopkins Verbal Learning Test-delayed recall, P = 0.001) and semantic memory (category fluency, P = 0.037). Clinical benefit occurred in the B-vitamin group for those in the upper quartile of homocysteine at baseline in global clinical dementia rating score (P = 0.02) and IQCODE score (P = 0.01). In this small intervention trial, B vitamins appear to slow cognitive and clinical decline in people with MCI, in particular in those with elevated homocysteine. Further trials are needed to see if this treatment will slow or prevent conversion from MCI to dementia. (ProQuest: ... denotes formulae/symbols omitted.) Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine-lowering treatment with B vitamins slows the rate of brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B vitamins on cognitive and clinical decline (secondary outcomes) in the same study. This was a double-blind, single-centre study, which included participants with MCI, aged ≥ 70 y, randomly assigned to receive a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B(12) and 20 mg vitamin B(6) (133 participants) or placebo (133 participants) for 2 y. Changes in cognitive or clinical function were analysed by generalized linear models or mixed-effects models. The mean plasma total homocysteine was 30% lower in those treated with B vitamins relative to placebo. B vitamins stabilized executive function (CLOX) relative to placebo (P = 0.015). There was significant benefit of B-vitamin treatment among participants with baseline homocysteine above the median (11.3 µmol/L) in global cognition (Mini Mental State Examination, P < 0.001), episodic memory (Hopkins Verbal Learning Test-delayed recall, P = 0.001) and semantic memory (category fluency, P = 0.037). Clinical benefit occurred in the B-vitamin group for those in the upper quartile of homocysteine at baseline in global clinical dementia rating score (P = 0.02) and IQCODE score (P = 0.01). In this small intervention trial, B vitamins appear to slow cognitive and clinical decline in people with MCI, in particular in those with elevated homocysteine. Further trials are needed to see if this treatment will slow or prevent conversion from MCI to dementia. |
| Author | de Jager, Celeste A. Oulhaj, Abderrahim Refsum, Helga Jacoby, Robin Smith, A. David |
| Author_xml | – sequence: 1 givenname: Celeste A. surname: de Jager fullname: de Jager, Celeste A. email: celeste.de-jager@ndm.ox.ac.uk, celeste.de-jager@ndm.ox.ac.uk organization: OPTIMA, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK – sequence: 2 givenname: Abderrahim surname: Oulhaj fullname: Oulhaj, Abderrahim organization: OPTIMA, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK – sequence: 3 givenname: Robin surname: Jacoby fullname: Jacoby, Robin organization: University Department of Psychiatry, Warneford Hospital, Oxford, UK – sequence: 4 givenname: Helga surname: Refsum fullname: Refsum, Helga organization: Department of Pharmacology, University of Oxford, Oxford, UK – sequence: 5 givenname: A. David surname: Smith fullname: Smith, A. David organization: Department of Pharmacology, University of Oxford, Oxford, UK |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25821808$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21780182$$D View this record in MEDLINE/PubMed |
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| Keywords | Prognosis Cognitive disorder Cognition B-Vitamins cognitive decline Folic acid Folate Intellectual deterioration Randomization cobalamin Homocystein Clinical trial Evolution Degenerative disease Human homocysteine Thiol Controlled therapeutic trial Pyridoxine Sulfur containing aminoacid Gerontology Treatment clinical dementia rating Cobalamine mild cognitive impairment Elderly Psychiatry Dementia Geriatrics |
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| References | Durga J, van Boxtel MP, Schouten EG, et al. 2007. Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomised, double blind, controlled trial. Lancet 369: 208-216. Morris JC. 1993. The Clinical Dementia Rating (CDR): current version and scoring rules. Neurology 43: 2412-2414. Obeid R, Herrmann W. 2006. Mechanisms of homocysteine neurotoxicity in neurodegenerative diseases with special reference to dementia. FEBS Lett 580: 2994-3005. Clarke R, Smith AD, Jobst KA, et al. 1998. Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 55: 1449-1455. Graham JE, Rockwood K, Beattie BL, et al. 1997. Prevalence and severity of cognitive impairment with and without dementia in an elderly population. Lancet 349: 1793-1796. Oulhaj A, Refsum H, Beaumont H, et al. 2010. Homocysteine as a predictor of cognitive decline in Alzheimer's disease. Int J Geriatr Psychiatry 25: 82-90. Smith AD, Smith SM, de Jager CA, et al. 2010. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment. A randomized controlled trial. PLoS One 5: e12244. Royall DR, Cordes JA, Polk M. 1998. CLOX: an executive clock drawing task. J Neurol Neurosurg Psychiatry 64: 588-594. McCaddon A. 2006. Homocysteine and cognition-a historical perspective. J Alzheimers Dis 9: 361-380. Seshadri S, Beiser A, Selhub J, et al. 2002. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N Engl J Med 346: 476-483. McGuinness B, Barrett SL, Craig D, Lawson J, Passmore AP. 2010. Executive functioning in Alzheimer's disease and vascular dementia. Int J Geriatr Psychiatry 25: 562-568. Jack CR, Petersen RC, Grundman M, et al. 2008. Longitudinal MRI findings from the vitamin E and donepezil treatment study for MCI. Neurobiol Aging 29: 1285-1295. Jorm AF. 2004. The Informant Questionnaire on cognitive decline in the elderly (IQCODE): a review. Int Psychogeriatr 16: 275-293. Stott DJ, Macintosh G, Lowe GD, et al. 2005. Randomized controlled trial of homocysteine-lowering vitamin treatment in elderly patients with vascular disease. Am J Clin Nutr 82: 1320-1326. Petersen RC. 2004. Mild cognitive impairment as a diagnostic entity. J Intern Med 256: 183-194. Smith AD. 2008. The worldwide challenge of the dementias: a role for B vitamins and homocysteine? Food Nutr Bull 29: S143-172. McCaddon A, Davies G, Hudson P, Tandy S, Cattell H. 1998. Total serum homocysteine in senile dementia of Alzheimer type. Int J Geriatr Psychiatry 13: 235-239. Aisen PS, Schneider LS, Sano M, et al. 2008. High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial. JAMA 300: 1774-1783. Selhub J, Bagley LC, Miller J, Rosenberg IH. 2000. B vitamins, homocysteine, and neurocognitive function in the elderly. Am J Clin Nutr 71: 614S-620S. Refsum H, Smith AD, Ueland PM, et al. 2004. Facts and recommendations about total homocysteine determinations: an expert opinion. Clin Chem 50: 3-32. Wedderburn C, Wear H, Brown J, et al. 2008. The utility of the Cambridge Behavioural Inventory in neurodegenerative disease. J Neurol Neurosurg Psychiatry 79: 500-503. Brandt J. 1991. The Hopkins Verbal Learning Test: development of a new memory test with six equivalent forms. Clin Neuropsychol 5: 125-142. Brandt J, Welsh KA, Breitner JC, et al. 1993. Hereditary influences on cognitive functioning in older men. A study of 4000 twin pairs. Arch Neurol 50: 599-603. McMahon JA, Green TJ, Skeaff CM, et al. 2006. A controlled trial of homocysteine lowering and cognitive performance. N Engl J Med 354: 2764-2772. Petersen RC, Roberts RO, Knopman DS, et al. 2009. Mild cognitive impairment: ten years later. Arch Neurol 66: 1447-1455. Wald DS, Kasturiratne A, Simmonds M. 2010. Effect of folic acid, with or without other B vitamins, on cognitive decline: meta-analysis of randomized trials. Am J Med 123: 522-527 e522. Folstein MF, Folstein SE, McHugh PR. 1975. 'Mini-mental state'. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 12: 189-198. Gauthier S, Reisberg B, Zaudig M, et al. 2006. Mild cognitive impairment. Lancet 367: 1262-1270. Roth M, Tym E, Mountjoy CQ, et al. 1986. CAMDEX: a standardised instrument for the diagnosis of mental disorder in the elderly with special reference to the early detection of dementia. Br J Psychiatry 149: 698-709. Morris JC, Heyman A, Mohs RC, et al. 1989. The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part I. Clinical and neuropsychological assessment of Alzheimer's disease. Neurology 39: 1159-1165. 2009; 66 2007; 369 1993; 43 2006; 9 2010; 123 1975; 12 2000; 71 2008; 79 2005; 82 2008; 300 1998; 64 2006; 354 1991; 5 2004; 50 1997; 349 2010; 25 1986; 149 2004; 256 1993; 50 2004; 16 2008; 29 2006; 580 2002; 346 2010; 5 1998; 55 2006; 367 1989; 39 1998; 13 e_1_2_8_28_1 e_1_2_8_29_1 e_1_2_8_24_1 e_1_2_8_26_1 e_1_2_8_27_1 e_1_2_8_3_1 e_1_2_8_2_1 e_1_2_8_5_1 e_1_2_8_4_1 e_1_2_8_7_1 Selhub J (e_1_2_8_25_1) 2000; 71 e_1_2_8_6_1 e_1_2_8_9_1 e_1_2_8_8_1 e_1_2_8_20_1 e_1_2_8_21_1 e_1_2_8_22_1 e_1_2_8_23_1 e_1_2_8_17_1 e_1_2_8_18_1 e_1_2_8_19_1 e_1_2_8_13_1 e_1_2_8_14_1 e_1_2_8_15_1 e_1_2_8_16_1 e_1_2_8_10_1 e_1_2_8_31_1 e_1_2_8_11_1 e_1_2_8_12_1 e_1_2_8_30_1 |
| References_xml | – reference: Graham JE, Rockwood K, Beattie BL, et al. 1997. Prevalence and severity of cognitive impairment with and without dementia in an elderly population. Lancet 349: 1793-1796. – reference: Wald DS, Kasturiratne A, Simmonds M. 2010. Effect of folic acid, with or without other B vitamins, on cognitive decline: meta-analysis of randomized trials. Am J Med 123: 522-527 e522. – reference: Jorm AF. 2004. The Informant Questionnaire on cognitive decline in the elderly (IQCODE): a review. Int Psychogeriatr 16: 275-293. – reference: Brandt J, Welsh KA, Breitner JC, et al. 1993. Hereditary influences on cognitive functioning in older men. A study of 4000 twin pairs. Arch Neurol 50: 599-603. – reference: Roth M, Tym E, Mountjoy CQ, et al. 1986. CAMDEX: a standardised instrument for the diagnosis of mental disorder in the elderly with special reference to the early detection of dementia. Br J Psychiatry 149: 698-709. – reference: Aisen PS, Schneider LS, Sano M, et al. 2008. High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial. JAMA 300: 1774-1783. – reference: Smith AD, Smith SM, de Jager CA, et al. 2010. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment. A randomized controlled trial. PLoS One 5: e12244. – reference: Refsum H, Smith AD, Ueland PM, et al. 2004. Facts and recommendations about total homocysteine determinations: an expert opinion. Clin Chem 50: 3-32. – reference: Clarke R, Smith AD, Jobst KA, et al. 1998. Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 55: 1449-1455. – reference: Oulhaj A, Refsum H, Beaumont H, et al. 2010. Homocysteine as a predictor of cognitive decline in Alzheimer's disease. Int J Geriatr Psychiatry 25: 82-90. – reference: Seshadri S, Beiser A, Selhub J, et al. 2002. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N Engl J Med 346: 476-483. – reference: Petersen RC, Roberts RO, Knopman DS, et al. 2009. Mild cognitive impairment: ten years later. Arch Neurol 66: 1447-1455. – reference: Gauthier S, Reisberg B, Zaudig M, et al. 2006. Mild cognitive impairment. Lancet 367: 1262-1270. – reference: Royall DR, Cordes JA, Polk M. 1998. CLOX: an executive clock drawing task. J Neurol Neurosurg Psychiatry 64: 588-594. – reference: McMahon JA, Green TJ, Skeaff CM, et al. 2006. A controlled trial of homocysteine lowering and cognitive performance. N Engl J Med 354: 2764-2772. – reference: Wedderburn C, Wear H, Brown J, et al. 2008. The utility of the Cambridge Behavioural Inventory in neurodegenerative disease. J Neurol Neurosurg Psychiatry 79: 500-503. – reference: Morris JC. 1993. The Clinical Dementia Rating (CDR): current version and scoring rules. Neurology 43: 2412-2414. – reference: McGuinness B, Barrett SL, Craig D, Lawson J, Passmore AP. 2010. Executive functioning in Alzheimer's disease and vascular dementia. Int J Geriatr Psychiatry 25: 562-568. – reference: Durga J, van Boxtel MP, Schouten EG, et al. 2007. Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomised, double blind, controlled trial. Lancet 369: 208-216. – reference: McCaddon A, Davies G, Hudson P, Tandy S, Cattell H. 1998. Total serum homocysteine in senile dementia of Alzheimer type. Int J Geriatr Psychiatry 13: 235-239. – reference: Smith AD. 2008. The worldwide challenge of the dementias: a role for B vitamins and homocysteine? Food Nutr Bull 29: S143-172. – reference: Brandt J. 1991. The Hopkins Verbal Learning Test: development of a new memory test with six equivalent forms. Clin Neuropsychol 5: 125-142. – reference: Jack CR, Petersen RC, Grundman M, et al. 2008. Longitudinal MRI findings from the vitamin E and donepezil treatment study for MCI. Neurobiol Aging 29: 1285-1295. – reference: Petersen RC. 2004. Mild cognitive impairment as a diagnostic entity. J Intern Med 256: 183-194. – reference: Selhub J, Bagley LC, Miller J, Rosenberg IH. 2000. B vitamins, homocysteine, and neurocognitive function in the elderly. Am J Clin Nutr 71: 614S-620S. – reference: Obeid R, Herrmann W. 2006. Mechanisms of homocysteine neurotoxicity in neurodegenerative diseases with special reference to dementia. FEBS Lett 580: 2994-3005. – reference: Stott DJ, Macintosh G, Lowe GD, et al. 2005. Randomized controlled trial of homocysteine-lowering vitamin treatment in elderly patients with vascular disease. Am J Clin Nutr 82: 1320-1326. – reference: Morris JC, Heyman A, Mohs RC, et al. 1989. The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part I. Clinical and neuropsychological assessment of Alzheimer's disease. Neurology 39: 1159-1165. – reference: Folstein MF, Folstein SE, McHugh PR. 1975. 'Mini-mental state'. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 12: 189-198. – reference: McCaddon A. 2006. Homocysteine and cognition-a historical perspective. 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Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine‐lowering treatment with... Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine-lowering treatment with B vitamins... |
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| SubjectTerms | Aged Aged, 80 and over Alzheimer's disease Biological and medical sciences Brain clinical dementia rating Clinical outcomes Clinical trials cobalamin Cognition - drug effects Cognition Disorders - blood Cognition Disorders - drug therapy Cognition Disorders - physiopathology cognitive decline Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Double-Blind Method Executive Function - drug effects Female folate Folic Acid - blood Folic Acid - therapeutic use General aspects Geriatric psychiatry Geriatrics Homocysteine Homocysteine - blood Humans Linear Models Male Medical sciences Memory - drug effects mild cognitive impairment Neurology Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry pyridoxine Risk factors Vitamin B Vitamin B 12 - blood Vitamin B 12 - therapeutic use Vitamin B 6 - blood Vitamin B 6 - therapeutic use Vitamin B Complex - blood Vitamin B Complex - therapeutic use |
| Title | Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial |
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