New Basis of the Neurotrophic Action of Vitamin B12
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Giuseppe Scalabrino
Abstract
Over the last few years we have reproduced all of the key morphological and biochemical features of human subacute combined degeneration in the central nervous system and peripheral nervous system of rats made cobalamin-deficient by means of total gastrectomy or a chronic cobalamin-deficient diet. We have also recently clarified the pathogenesis of experimental subacute combined degeneration induced in the rat by cobalamin deprivation. The results of our studies strongly support the notion that cobalamin plays a pivotal role in regulating the balance of the network of cytokines and growth factors in the central nervous system of the rat. We have demonstrated that cobalamin tightly regulates the central nervous system synthesis and/or the cerebrospinal fluid level of two cytokines, tumor necrosis factor-αand interleukin-6, and a growth factor, epidermal growth factor. Of these neuroactive agents, one, tumor necrosis factor-α, is neurotoxic, whereas the others are neurotrophic. Therefore, it becomes clear that cobalamin-deficient central neuropathy is caused not by the withdrawal of the vitamin, but reflects a locally increased production of neurotoxic agents, combined with the locally decreased production of neurotrophic agents.
Copyright © 2003 by Walter de Gruyter GmbH & Co. KG
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- Meetings and Awards
Articles in the same Issue
- Where Are We Standing in Homocysteine Research?
- DACH-LIGA Homocystein (German, Austrian and Swiss Homocysteine Society): Consensus Paper on the Rational Clinical Use of Homocysteine, Folic Acid and B-Vitamins in Cardiovascular and Thrombotic Diseases: Guidelines and Recommendations
- Hyperhomocysteinaemia as a Risk Factor for Venous Thrombosis: An Update of the Current Evidence
- Does Homocysteine Cause Hypertension?
- Homocysteine Metabolism in Renal Disease
- Hyperhomocysteinemia and B-Vitamin Deficiencies in Infants and Children
- The Role of Genetic Factors in the Development of Hyperhomocysteinemia
- New Basis of the Neurotrophic Action of Vitamin B12
- Hyperhomocysteinemia and Immune Activation
- Interactions of Homocysteine, Nitric Oxide, Folate and Radicals in the Progressively Damaged Endothelium
- Influence of Hyperhomocysteinemia on the Cellular Redox State – Impact on Homocysteine-Induced Endothelial Dysfunction
- Homocysteine-Thiolactone and S-Nitroso-Homocysteine Mediate Incorporation of Homocysteine into Protein in Humans
- Association of Asymmetric Dimethylarginine and Endothelial Dysfunction
- Genetic Determinants of Folate and Vitamin B12 Metabolism: A Common Pathway in Neural Tube Defect and Down Syndrome?
- Functional Vitamin B12 Deficiency and Determination of Holotranscobalamin in Populations at Risk
- Holotranscobalamin as a Predictor of Vitamin B12 Status
- Hyperhomocysteinemia and B-Vitamin Status after Discontinuation of Oral Anticoagulation Therapy in Patients with a History of Venous Thromboembolism
- Measurement of Carotid Plaque and Effect of Vitamin Therapy for Total Homocysteine
- Folate Improves Endothelial Function in Patients with Coronary Heart Disease
- The Impact of Hyperhomocysteinemia as a Cardiovascular Risk Factor in the Prediction of Coronary Heart Disease
- Homocysteine Increases during Endurance Exercise
- Comparison of the Influence of Volume-Oriented Training and High-Intensity Interval Training on Serum Homocysteine and Its Cofactors in Young, Healthy Swimmers
- Analysis of the Transcobalamin II 776C>G (259P>R) Single Nucleotide Polymorphism by Denaturing HPLC in Healthy Elderly: Associations with Cobalamin, Homocysteine and Holo-Transcobalamin II
- Meetings and Awards
