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Open AccessJournal ArticleDOI

Consistent decrease in global DNA methylation and hydroxymethylation in the hippocampus of Alzheimer's disease patients.

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TLDR
Human postmortem results strengthen the notion that AD is associated with alterations in DNA methylation and hydroxymethylation, and provide a basis for further epigenetic studies identifying the exact genetic loci with aberrant epigenetic signatures.
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This article is published in Neurobiology of Aging.The article was published on 2013-09-01 and is currently open access. It has received 351 citations till now. The article focuses on the topics: DNA Hydroxymethylation & DNA methylation.

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Book ChapterDOI

Twin studies on the epigenetics of selected neurological disorders and carotid artery disease

TL;DR: This chapter reviews the results of twin studies assessing epigenetic influence on these neurological conditions and the results are compared to those yielded on non-twin samples and the possible future therapeutic implications are discussed.
Book ChapterDOI

Neurochemical Aspects of Alzheimer Disease

TL;DR: Accumulating evidence suggests that AD also involves increases in metal ions, nitric oxide generation, reduction in expression of trophic factors, dysfunction of the ubiquitin–proteasome system, depletion of endogenous antioxidants, and expression of proapoptotic proteins leading to synaptic and neuronal loss.
Book ChapterDOI

Epigenetics and cerebrovascular diseases

TL;DR: This chapter focuses on stroke-related epigenetic mechanisms described to date, especially DNA methylation, and cardiovascular risk factors that modulate the risk of stroke.

Epigenetic Dysregulation in the Basocortical Cholinergic Projection System During the Progression of Alzheimer's Disease

TL;DR: In an effort to characterize alterations in the basocortical phenotype, semi-quantitative western blotting and immunohistochemistry were utilized to evaluate histone deacetylase (HDAC) and sirtuin(SIRT) levels in individuals that died with a premortem clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment, mild cognitive impairment, mild/moderate AD, or severe AD (sAD) as discussed by the authors.
Book ChapterDOI

Personalized Medicine and Epigenetic Drug Development

TL;DR: A link has been established between nutrition and epigenetics, in which drastic dietary modifications have shown changes in epigenetic mechanisms also affecting prevention and treatment of disease.
References
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Journal ArticleDOI

Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals

TL;DR: Advances in the understanding of the mechanism and role of DNA methylation in biological processes are reviewed, showing that epigenetic mechanisms seem to allow an organism to respond to the environment through changes in gene expression.
Journal ArticleDOI

Conversion of 5-Methylcytosine to 5-Hydroxymethylcytosine in Mammalian DNA by MLL Partner TET1

TL;DR: It is shown here that TET1, a fusion partner of the MLL gene in acute myeloid leukemia, is a 2-oxoglutarate (2OG)- and Fe(II)-dependent enzyme that catalyzes conversion of 5mC to 5-hydroxymethylcytosine (hmC) in cultured cells and in vitro.
Journal ArticleDOI

Alzheimer's Disease Is a Synaptic Failure

TL;DR: Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfunction is caused by diffusible oligomeric assemblies of the amyloid β protein.
Journal ArticleDOI

The Nuclear DNA Base 5-Hydroxymethylcytosine Is Present in Purkinje Neurons and the Brain

TL;DR: It is shown that, as well as 5mC in mammalian genomes, there are also significant amounts of 5-hydroxymethylcytosine (5hmC) in DNA of Purkinje neurons, which have large nuclei with apparently very little heterochromatin.
Journal ArticleDOI

Linking DNA methylation and histone modification: patterns and paradigms

TL;DR: Relationships between DNA methylation and histone modification have implications for understanding normal development as well as somatic cell reprogramming and tumorigenesis.
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