Understanding the Genome: Implications for Human Nutrition?

Troesch, Barbara; Hoeft, B

doi:10.4172/2376-1318.1000e133

Cited by 1 publication

(1 citation statement)

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“…Insufficiency of B-vitamins may also affect the development of the diseases via their role in DNA methylation [16], synthesis and/or repair [17] or in modulating neurotransmission [18]. Polymorphisms in genes encoding for specific enzymes can significantly affect their activity [19]. Therefore, studying mutations at critical steps in the metabolism of B-vitamins might help resolve some of the inconsistencies reported for their protective effect on the development of AD.…”

Section: Introductionmentioning

confidence: 99%

Potential Links between Impaired One-Carbon Metabolism Due to Polymorphisms, Inadequate B-Vitamin Status, and the Development of Alzheimer’s Disease

Troesch¹,

Weber²,

Mohajeri³

2016

Nutrients

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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.

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