Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease
Alzheimer’s disease (AD) is the major cause of dementia and no preventive or effective treatment has been established to date. The etiology of AD is poorly understood, but genetic and environmental factors seem to play a role in its onset and progression. In particular, factors affecting the one-car...
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doaj-8c7b05ee23ff43d4acf68ce02c2dfb732020-11-24T22:31:24ZengMDPI AGNutrients2072-66432016-12-0181280310.3390/nu8120803nu8120803Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s DiseaseBarbara Troesch0Peter Weber1M. Hasan Mohajeri2DSM Nutritional Products Ltd., Wurmisweg 576, Kaiseraugst 4303, SwitzerlandDSM Nutritional Products Ltd., Wurmisweg 576, Kaiseraugst 4303, SwitzerlandDSM Nutritional Products Ltd., Wurmisweg 576, Kaiseraugst 4303, SwitzerlandAlzheimer’s disease (AD) is the major cause of dementia and no preventive or effective treatment has been established to date. The etiology of AD is poorly understood, but genetic and environmental factors seem to play a role in its onset and progression. In particular, factors affecting the one-carbon metabolism (OCM) are thought to be important and elevated homocysteine (Hcy) levels, indicating impaired OCM, have been associated with AD. We aimed at evaluating the role of polymorphisms of key OCM enzymes in the etiology of AD, particularly when intakes of relevant B-vitamins are inadequate. Our review indicates that a range of compensatory mechanisms exist to maintain a metabolic balance. However, these become overwhelmed if the activity of more than one enzyme is reduced due to genetic factors or insufficient folate, riboflavin, vitamin B6 and/or vitamin B12 levels. Consequences include increased Hcy levels and reduced capacity to synthetize, methylate and repair DNA, and/or modulated neurotransmission. This seems to favor the development of hallmarks of AD particularly when combined with increased oxidative stress e.g., in apolipoprotein E (ApoE) ε4 carriers. However, as these effects can be compensated at least partially by adequate intakes of B-vitamins, achieving optimal B-vitamin status for the general population should be a public health priority.http://www.mdpi.com/2072-6643/8/12/803homocysteinedementiaAlzheimer’s diseasenutritionone-carbon metabolismB-vitaminspolymorphismpreventiontherapy |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Barbara Troesch Peter Weber M. Hasan Mohajeri |
spellingShingle |
Barbara Troesch Peter Weber M. Hasan Mohajeri Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease Nutrients homocysteine dementia Alzheimer’s disease nutrition one-carbon metabolism B-vitamins polymorphism prevention therapy |
author_facet |
Barbara Troesch Peter Weber M. Hasan Mohajeri |
author_sort |
Barbara Troesch |
title |
Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease |
title_short |
Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease |
title_full |
Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease |
title_fullStr |
Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease |
title_full_unstemmed |
Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease |
title_sort |
potential links between impaired one-carbon metabolism due to polymorphisms, inadequate b-vitamin status, and the development of alzheimer’s disease |
publisher |
MDPI AG |
series |
Nutrients |
issn |
2072-6643 |
publishDate |
2016-12-01 |
description |
Alzheimer’s disease (AD) is the major cause of dementia and no preventive or effective treatment has been established to date. The etiology of AD is poorly understood, but genetic and environmental factors seem to play a role in its onset and progression. In particular, factors affecting the one-carbon metabolism (OCM) are thought to be important and elevated homocysteine (Hcy) levels, indicating impaired OCM, have been associated with AD. We aimed at evaluating the role of polymorphisms of key OCM enzymes in the etiology of AD, particularly when intakes of relevant B-vitamins are inadequate. Our review indicates that a range of compensatory mechanisms exist to maintain a metabolic balance. However, these become overwhelmed if the activity of more than one enzyme is reduced due to genetic factors or insufficient folate, riboflavin, vitamin B6 and/or vitamin B12 levels. Consequences include increased Hcy levels and reduced capacity to synthetize, methylate and repair DNA, and/or modulated neurotransmission. This seems to favor the development of hallmarks of AD particularly when combined with increased oxidative stress e.g., in apolipoprotein E (ApoE) ε4 carriers. However, as these effects can be compensated at least partially by adequate intakes of B-vitamins, achieving optimal B-vitamin status for the general population should be a public health priority. |
topic |
homocysteine dementia Alzheimer’s disease nutrition one-carbon metabolism B-vitamins polymorphism prevention therapy |
url |
http://www.mdpi.com/2072-6643/8/12/803 |
work_keys_str_mv |
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