Role of epigenetics in Alzheimer's and Parkinson's disease

被引:78
|
作者
Kwok, John B. J. [1 ,2 ]
机构
[1] Univ New S Wales, Kensington, NSW 2033, Australia
[2] Neurosci Res Australia, Randwick, NSW, Australia
关键词
Alzheimer's disease; DNA methylation; epistasis; gene-environment interaction; histone deacetylase inhibitor; Parkinson's disease; SNP; AMYLOID PRECURSOR PROTEIN; GLYCOGEN-SYNTHASE KINASE-3-BETA; GENOMIC DNA METHYLATION; TAU GENES INTERACT; ALPHA-SYNUCLEIN; MISSENSE MUTATIONS; HISTONE ACETYLATION; COLORECTAL-CANCER; OXIDATIVE STRESS; APOLIPOPROTEIN-E;
D O I
10.2217/EPI.10.43
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Alzheimer's disease (AD) and Parkinson's disease (PD) are two common neurodegenerative diseases that result in the progressive damage or death of neurons. Environmental agents have the potential to damage the developing and mature nervous system, resulting in neurodegenerative diseases. Heritable changes in gene expression that do not involve coding sequence modifications are referred to as 'epigenetic'. These modifications include DNA methylation and downstream modification of histones. Environmental factors, including heavy metals and dietary folate intake, perturb neurodegenerative genes by epigenetic means, leading to altered gene expression and late-onset neurodegenerative diseases. Research into the genetic control of DNA methylation indicates an allelic skewing in a significant proportion of genes. This phenomenon may determine how an individual's genetic makeup can alter the effect an environmental factor has on their risk of developing neurodegeneration. Finally, preliminary evidence using cell culture and transgenic animal models suggests that whole classes of pan-epigenetic modifiers will have significant protective effects against common neurodegenerative diseases.
引用
收藏
页码:671 / 682
页数:12
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