The 'golden age' of DNA methylation in neurodegenerative diseases

Andrea Fuso

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

DNA methylation reactions are regulated, in the first instance, by enzymes and the intermediates that constitute the 'so called' one-carbon metabolism. This is a complex biochemical pathway, also known as the homocysteine cycle, regulated by the presence of B vitamins (folate, B6, B12) and choline, among other metabolites. One of the intermediates of this metabolism is S-adenosylmethionine, which represent the methyl donor in all the DNA methyltransferase reactions in eukaryotes. The one-carbon metabolism therefore produces the substrate necessary for the transferring of a methyl group on the cytosine residues of DNA; S-adenosylmethionine also regulates the activity of the enzymes that catalyze this reaction, namely the DNA methyltransferases (DNMTs). Alterations of this metabolic cycle can therefore be responsible for aberrant DNA methylation processes possibly leading to several human diseases. As a matter of fact, increasing evidences indicate that a number of human diseases with multifactorial origin may have an epigenetic basis. This is also due to the great technical advances in the field of epigenetic research. Among the human diseases associated with epigenetic factors, aging-related and neurodegenerative diseases are probably the object of most intense research. This review will present the main evidences linking several human diseases to DNA methylation, with particular focus on neurodegenerative diseases, together with a short description of the state-of-the-art of methylation assays.

Original languageEnglish
Pages (from-to)523-534
Number of pages12
JournalClinical Chemistry and Laboratory Medicine
Volume51
Issue number3
DOIs
Publication statusPublished - Mar 2013

Fingerprint

Neurodegenerative diseases
DNA Methylation
Neurodegenerative Diseases
Metabolism
Epigenomics
S-Adenosylmethionine
Methyltransferases
DNA
Carbon
Vitamin B Complex
Vitamin B 6
Methylation
Cytosine
Homocysteine
Enzymes
Metabolites
Choline
Eukaryota
Folic Acid
Research

Keywords

  • DNA methylation
  • Epigenetic assays
  • Epigenetics
  • Human disease
  • Neurodegeneration
  • One-carbon metabolism

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

The 'golden age' of DNA methylation in neurodegenerative diseases. / Fuso, Andrea.

In: Clinical Chemistry and Laboratory Medicine, Vol. 51, No. 3, 03.2013, p. 523-534.

Research output: Contribution to journalArticle

@article{16e52b8d47454acfb90a896a6a26b176,
title = "The 'golden age' of DNA methylation in neurodegenerative diseases",
abstract = "DNA methylation reactions are regulated, in the first instance, by enzymes and the intermediates that constitute the 'so called' one-carbon metabolism. This is a complex biochemical pathway, also known as the homocysteine cycle, regulated by the presence of B vitamins (folate, B6, B12) and choline, among other metabolites. One of the intermediates of this metabolism is S-adenosylmethionine, which represent the methyl donor in all the DNA methyltransferase reactions in eukaryotes. The one-carbon metabolism therefore produces the substrate necessary for the transferring of a methyl group on the cytosine residues of DNA; S-adenosylmethionine also regulates the activity of the enzymes that catalyze this reaction, namely the DNA methyltransferases (DNMTs). Alterations of this metabolic cycle can therefore be responsible for aberrant DNA methylation processes possibly leading to several human diseases. As a matter of fact, increasing evidences indicate that a number of human diseases with multifactorial origin may have an epigenetic basis. This is also due to the great technical advances in the field of epigenetic research. Among the human diseases associated with epigenetic factors, aging-related and neurodegenerative diseases are probably the object of most intense research. This review will present the main evidences linking several human diseases to DNA methylation, with particular focus on neurodegenerative diseases, together with a short description of the state-of-the-art of methylation assays.",
keywords = "DNA methylation, Epigenetic assays, Epigenetics, Human disease, Neurodegeneration, One-carbon metabolism",
author = "Andrea Fuso",
year = "2013",
month = "3",
doi = "10.1515/cclm-2012-0618",
language = "English",
volume = "51",
pages = "523--534",
journal = "Clinical Chemistry and Laboratory Medicine",
issn = "1434-6621",
publisher = "Walter de Gruyter GmbH",
number = "3",

}

TY - JOUR

T1 - The 'golden age' of DNA methylation in neurodegenerative diseases

AU - Fuso, Andrea

PY - 2013/3

Y1 - 2013/3

N2 - DNA methylation reactions are regulated, in the first instance, by enzymes and the intermediates that constitute the 'so called' one-carbon metabolism. This is a complex biochemical pathway, also known as the homocysteine cycle, regulated by the presence of B vitamins (folate, B6, B12) and choline, among other metabolites. One of the intermediates of this metabolism is S-adenosylmethionine, which represent the methyl donor in all the DNA methyltransferase reactions in eukaryotes. The one-carbon metabolism therefore produces the substrate necessary for the transferring of a methyl group on the cytosine residues of DNA; S-adenosylmethionine also regulates the activity of the enzymes that catalyze this reaction, namely the DNA methyltransferases (DNMTs). Alterations of this metabolic cycle can therefore be responsible for aberrant DNA methylation processes possibly leading to several human diseases. As a matter of fact, increasing evidences indicate that a number of human diseases with multifactorial origin may have an epigenetic basis. This is also due to the great technical advances in the field of epigenetic research. Among the human diseases associated with epigenetic factors, aging-related and neurodegenerative diseases are probably the object of most intense research. This review will present the main evidences linking several human diseases to DNA methylation, with particular focus on neurodegenerative diseases, together with a short description of the state-of-the-art of methylation assays.

AB - DNA methylation reactions are regulated, in the first instance, by enzymes and the intermediates that constitute the 'so called' one-carbon metabolism. This is a complex biochemical pathway, also known as the homocysteine cycle, regulated by the presence of B vitamins (folate, B6, B12) and choline, among other metabolites. One of the intermediates of this metabolism is S-adenosylmethionine, which represent the methyl donor in all the DNA methyltransferase reactions in eukaryotes. The one-carbon metabolism therefore produces the substrate necessary for the transferring of a methyl group on the cytosine residues of DNA; S-adenosylmethionine also regulates the activity of the enzymes that catalyze this reaction, namely the DNA methyltransferases (DNMTs). Alterations of this metabolic cycle can therefore be responsible for aberrant DNA methylation processes possibly leading to several human diseases. As a matter of fact, increasing evidences indicate that a number of human diseases with multifactorial origin may have an epigenetic basis. This is also due to the great technical advances in the field of epigenetic research. Among the human diseases associated with epigenetic factors, aging-related and neurodegenerative diseases are probably the object of most intense research. This review will present the main evidences linking several human diseases to DNA methylation, with particular focus on neurodegenerative diseases, together with a short description of the state-of-the-art of methylation assays.

KW - DNA methylation

KW - Epigenetic assays

KW - Epigenetics

KW - Human disease

KW - Neurodegeneration

KW - One-carbon metabolism

UR - http://www.scopus.com/inward/record.url?scp=84882417694&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84882417694&partnerID=8YFLogxK

U2 - 10.1515/cclm-2012-0618

DO - 10.1515/cclm-2012-0618

M3 - Article

VL - 51

SP - 523

EP - 534

JO - Clinical Chemistry and Laboratory Medicine

JF - Clinical Chemistry and Laboratory Medicine

SN - 1434-6621

IS - 3

ER -