Plasma A , homocysteine, and cognition: The Vitamin Intervention for Stroke Prevention (VISP) trial
| Autor: | B. T. Hyman, M. Stampfer, Michael C. Irizarry, S.M. Greenberg, Anand Viswanathan, S. Campbell, S. Raj |
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| Rok vydání: | 2009 |
| Předmět: |
Male
Vitamin medicine.medical_specialty Homocysteine Down-Regulation Cobalamin chemistry.chemical_compound Cognition Folic Acid Double-Blind Method Internal medicine mental disorders medicine Humans Treatment Failure Vitamin B12 Cyanocobalamin Stroke Aged Amyloid beta-Peptides Dose-Response Relationship Drug business.industry Osmolar Concentration Pyridoxine Vitamins Articles Middle Aged medicine.disease Peptide Fragments nervous system diseases Vitamin B 12 Endocrinology chemistry Vitamin B Complex Female Neurology (clinical) Alzheimer's disease business medicine.drug |
| Zdroj: | Neurology. 72:268-272 |
| ISSN: | 1526-632X 0028-3878 |
| DOI: | 10.1212/01.wnl.0000339486.63862.db |
| Popis: | Background: Amyloid-beta protein (Aβ) plays a key role in Alzheimer disease (AD) and is also implicated in cerebral small vessel disease. Serum total homocysteine (tHcy) is a risk factor for small vessel disease and cognitive impairment and correlates with plasma Aβ levels. To determine whether this association results from a common pathophysiologic mechanism, we investigated whether vitamin supplementation–induced reduction of tHcy influences plasma Aβ levels in the Vitamin Intervention in Stroke Prevention (VISP) study. Methods: Two groups of 150 patients treated with either the high-dose or low-dose formulation of pyridoxine, cobalamin, and folic acid in a randomized, double-blind fashion were selected among the participants in the VISP study without recurrent stroke during follow-up and in the highest 10% of the distribution for baseline tHcy levels. Concentrations of plasma Aβ with 40 (Aβ40) and 42 (Aβ42) amino acids were measured at baseline and at the 2-year visit. Results: tHcy levels significantly decreased with vitamin supplementation in both groups. tHcy were strongly correlated with Aβ40 but not Aβ42 concentrations. There was no difference in the change in Aβ40, Aβ42 ( p = 0.40, p = 0.35), or the Aβ42/Aβ40 ratio over time ( p = 0.86) between treatment groups. Aβ measures were not associated with cognitive change. Conclusions: This double-blind randomized controlled trial of vitamin therapy demonstrates a strong correlation between serum tHcy and plasma Aβ40 concentrations in subjects with ischemic stroke. Treatment with high dose vitamins does not, however, influence plasma levels of Aβ, despite their effect on lowering tHcy. Our results suggest that although tHcy is associated with plasma Aβ40, they may be regulated by independent mechanisms. |
| Databáze: | OpenAIRE |
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