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The massive changes in gene expression that occur during developmental transitions rely at least in part on epigenetic processes such as chromatin remodeling to establish specific states for gene expression.
Also, we cannot ignore genetic influences on epigenetic processes.
Several studies have investigated the impact of Se on epigenetic processes.
Environmental influences on eukaryotic cell growth, proliferation, and development have well-documented effects on epigenetic processes [ 1, 2].
Both animal and human studies reveal effects on placental function [ 70], the development of fetal organ function and on epigenetic processes in the offspring early in development [ 71].
So far, the majority of reports in this area have been proof-of-principle studies in experimental models, although there have been some recent reports on the effect of early life environment on epigenetic processes in humans.
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More recent discoveries on functional mechanisms of epigenetic processes indicate that most of these epigenetic processes are heritable.
However, during the past years of research, it has become more and more evident that the influence of epigenetic processes on the development of rheumatic diseases is probably as strong as the genetic background of a patient.
In this review, I will give an overview on the current knowledge of epigenetic processes in memory function and brain disease with a focus on Morbus Alzheimer as the most common neurodegenerative disease.
While the greatest attention has been on folate in respect of epigenetic processes, it seems likely that vitamins B2, B6, B12 and preformed methionine are also potentially important.
Our knowledge on the epigenetic status and dynamics of epigenetic processes regulating the SLC6A3 and the SLC6A4 is very limited due to significant technological challenges; therefore, systematic identification of possible targets amenable to epigenetic modifications by computational means intrinsically is worthwhile.
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