Journal article
Deficits in Spermatogenesis but not Neurogenesis are Alleviated by Chronic Testosterone Therapy in R6/1 Huntington's Disease Mice
AJ Hannan, MI Ransome
Journal of Neuroendocrinology | WILEY | Published : 2012
Abstract
Despite the well established central pathophysiology of Huntington's disease (HD), less is known about systemic impairments that are emerging as significant contributors to the morbidity of this neurodegenerative condition. Given the evidence of neuroendocrine dysfunction in HD patients and the pro-neural properties of sex-hormones, we explored the therapeutic potential of hormone therapy in the HD R6/1 mouse model (HD mice). HD mice over-express exon-1 of the defective human HD gene and replicate many of the clinical behavioural, biochemical and physiological impairments. Seven-week-old HD and wild-type littermate mice had either saline (control) or testosterone (treatment; 160μg/day over 9..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
National Health and Medical Research Council Project Grant Number: 509031 (A.J.H.). M. I. R. is supported by a National Health and Medical Research Council Australian Biomedical Fellowship (ID: 628868) and A.J.H. is supported by a Australian Research Council Future Fellowship and is an Honorary National Health and Medical Research Council Senior Research Fellow. We wish to thank Wah Chin Boon for her aid in the preparation of this manuscript. The authors declare that there are no conflicts of interest.