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Chromatin Acetylation Status in the Manifestation of Neurodegenerative Diseases

HDAC inhibitors as therapeutic tools

  • Chapter
Chromatin and Disease

Part of the book series: Subcellular Biochemistry ((SCBI,volume 41))

During the development and maintenance of the central nervous system, neurons receive specific instructions to differentiate, survive or die, the correct choice being crucial for the maturation of a functional brain and to face pathological conditions. At the transcriptional level, chromatin remodeling enzymes participates in such processes. In this paper, we will see that disruption of the Histone acetyl transferase (HAT)/Deacetylase (HDAC) balance is often observed in different contexts of neurological disorders and more particularly during neuronal apoptosis. During the last 5 years, it has been evidenced that the chromatin acetylation status was greatly impaired in different neurodegenerative diseases, a common mechanism being the loss of function of a specific HAT: the CREB-binding protein (CBP). We will review the last attempts of the use of small molecules antagonizing HDAC activity (HDAC inhibitors) to restore proper levels of acetylation and enhance neuronal survival, both in in vitro and in vivo models of neurodegenerative diseases such as polyglutamine-related diseases and amyotrophic lateral sclerosis. Although this strategy lacks specificity towards CBP, certain of these molecules display promising therapeutic properties

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Authors and Affiliations

  1. Laboratoire de Signalisation Moléculaire et Neurodégénérescence – INSERM U692 11, rue Humann, 67085 Strasbourg Cedex, France

    Boutillier Anne-Laurence, Rouaux Caroline, Panteleeva Irina & Loeffler Jean-Philippe

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  1. Boutillier Anne-Laurence
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  2. Rouaux Caroline
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  3. Panteleeva Irina
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  4. Loeffler Jean-Philippe
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Editor information

Editors and Affiliations

  1. Jawaharlal Centre for Advanced Scientific Research, Jakkur, Bangalore, India

    Tapas K. Kundu

  2. Queens College,City University of New York, New York, USA

    R. Bittman

  3. Saha Institute of Nuclear Physics, Calcutta, India

    D. Dasgupta

  4. Max-Planck-Institute for Biochemistry, Munich, Germany

    H. Engelhardt

  5. MOLISA GmbH, Magdeburg, Germany

    L. Flohe

  6. German Cancer Research Center, Heidelberg, Germany

    H. Herrmann

  7. Texas A & M University, Texas, USA

    A. Holzenburg

  8. National University of Ireland, Galway, Ireland

    H-P. Nasheuer

  9. The Hebrew University, Jerusalem, Israel

    S. Rottem

  10. DSM Nutritional Products Ltd, Basel, Switzerland

    M. Wyss

  11. Max-Planck-Institute for Biochemistry, Munich, Germany

    P. Zwickl

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Anne-Laurence, B., Caroline, R., Irina, P., Jean-Philippe, L. (2007). Chromatin Acetylation Status in the Manifestation of Neurodegenerative Diseases. In: Kundu, T.K., et al. Chromatin and Disease. Subcellular Biochemistry, vol 41. Springer, Dordrecht. https://doi.org/10.1007/1-4020-5466-1_12

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