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Hypothesis and Theory ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Cell. Neurosci. | doi: 10.3389/fncel.2018.00037

Reactive neuroblastosis in Huntington’s disease: A putative therapeutic target for striatal regeneration in the adult brain

Mahesh Kandasamy1* and  Ludwig Aigner2*
  • 1Bharathidasan University, India
  • 2Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Austria

The cellular and molecular mechanisms underlying the reciprocal relationship between adult neurogenesis, cognitive and motor functions have been an important focus of investigation in the establishment of effective neural replacement therapies for neurodegenerative disorders. While neuronal loss, reactive gliosis and defects in the self-repair capacity have extensively been characterized in neurodegenerative disorders, the transient excess production of neuroblasts detected in the adult striatum of animal models of Huntington’s disease (HD) and in post-mortem brain of HD patients, has only marginally been addressed. This abnormal cellular response in the striatum appears to originate from the selective proliferation and ectopic migration of neuroblasts derived from the SVZ. Based on and in line with the term “reactive astrogliosis”, we propose to name the observed cellular event “reactive neuroblastosis”. Although, the functional relevance of reactive neuroblastosis is unknown, we speculate that this process may provide support for the tissue regeneration in compensating the structural and physiological functions of the striatum in lieu of ageing or of the neurodegenerative process. Thus, in this review, we comprehend different possibilities for the regulation of striatal neurogenesis, neuroblastosis and their functional relevance in the context of HD.

Keywords: adult neurogenesis, Huntington's disease, Striatum, Reactive neuroblastosis, Doublecortin.

Received: 16 Nov 2017; Accepted: 31 Jan 2018.

Edited by:

Satoshi Goto, Tokushima University, Japan

Reviewed by:

Henry J. Waldvogel, University of Auckland, New Zealand
Nickolay Brustovetsky, School of Medicine, Indiana University Bloomington, United States  

Copyright: © 2018 Kandasamy and Aigner. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Dr. Mahesh Kandasamy, Bharathidasan University, Tiruchirappalli, India, pkmahesh5@googlemail.com
Prof. Ludwig Aigner, Paracelsus Medical University, Institute of Molecular Regenerative Medicine, Strubergasse 21, Salzburg, 5020, Austria, ludwig.aigner@pmu.ac.at