The latent stem cell population is retained in the hippocampus of transgenic Huntington's disease mice but not wild-type mice

• Published in: PloS one Vol. 6; no. 3; p. e18153
• Main Authors: Walker, Tara L, Turnbull, Geoff W, Mackay, Eirinn W, Hannan, Anthony J, Bartlett, Perry F
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 24.03.2011; Public Library of Science (PLoS)
• Subjects: Age; Animal cognition; Animals; Biology; Brain; Brain-derived neurotrophic factor; Cell Differentiation - genetics; Cell Differentiation - physiology; Cell growth; Exercise; Female; Florey, Howard; Genetic engineering; Growth factors; Health aspects; High definition television; Hippocampus; Hippocampus - metabolism; Hippocampus - pathology; Huntington Disease - genetics; Huntington Disease - metabolism; Huntington Disease - pathology; Huntington's disease; Huntingtons disease; Immunohistochemistry; Maintenance; Medicine; Mice; Mice, Inbred BALB C; Mice, Transgenic; Neurogenesis; Neurogenesis - genetics; Neurogenesis - physiology; Population; Rodents; Stem cell transplantation; Stem cells; Stem Cells - metabolism; Stem Cells - pathology; Subventricular zone; Transgenic animals; Transgenic mice; Sydney New South Wales Australia; Melbourne Victoria Australia; Queensland Australia; Australia
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0018153

The demonstration of the brain's ability to initiate repair in response to disease or injury has sparked considerable interest in therapeutic strategies to stimulate adult neurogenesis. In this study we examined the effect of a progressive neurodegenerative condition on neural precursor activity in the subventricular zone (SVZ) and hippocampus of the R6/1 transgenic mouse model of Huntington's disease (HD). Our results revealed an age-related decline in SVZ precursor numbers in both wild-type (WT) and HD mice. Interestingly, hippocampal precursor numbers declined with age in WT mice, although we observed maintenance in hippocampal precursor number in the HD animals in response to advancement of the disease. This maintenance was consistent with activation of a recently identified latent hippocampal precursor population. We found that the small latent stem cell population was also maintained in the HD hippocampus at 33 weeks, whereas it was not present in the WT. Our findings demonstrate that, despite a loss of neurogenesis in the HD hippocampus in vivo, there is a unique maintenance of the precursor and stem cells, which may potentially be activated to ameliorate disease symptoms.