Epigenetic Changes in Neurodegenerative Diseases

Afflicted neurons in various neurodegenerative diseases generally display diverse and complex pathological features before catastrophic occurrence of massive neuronal loss at the late stages of the diseases. This complex nature of neuronal pathophysiology inevitably implicates systemwide changes in...

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Published inMolecules and cells Vol. 39; no. 11; pp. 783 - 789
Main Authors Kwon, Min Jee, Kim, Sunhong, Han, Myeong Hoon, Lee, Sung Bae
Format Journal Article
LanguageEnglish
Published United States Korean Society for Molecular and Cellular Biology 30.11.2016
한국분자세포생물학회
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Summary:Afflicted neurons in various neurodegenerative diseases generally display diverse and complex pathological features before catastrophic occurrence of massive neuronal loss at the late stages of the diseases. This complex nature of neuronal pathophysiology inevitably implicates systemwide changes in basic cellular activities such as transcriptional controls and signal cascades, and so on, as a cause. Recently, as one of these systemwide cellular changes associated with neurodegenerative diseases, epigenetic changes caused by protein toxicity have begun to be highlighted. Notably, recent advances in related techniques including next-generation sequencing (NGS) and mass spectrometry enable us to monitor changes in the post-translational modifications (PTMs) of histone proteins and to link these changes in histone PTMs to the specific transcriptional changes. Indeed, epigenetic alterations and consequent changes in neuronal transcriptome are now begun to be extensively studied in neurodegenerative diseases including Alzheimer's disease (AD). In this review, we will discuss details of our current understandings on epigenetic changes associated with two representative neurodegenerative diseases [AD and polyglutamine (polyQ) diseases] and further discuss possible future development of pharmaceutical treatment of the diseases through modulating these epigenetic changes.
Bibliography:These authors contributed equally to this work.
G704-000079.2016.39.11.004
ISSN:1016-8478
0219-1032
DOI:10.14348/molcells.2016.0233