Journal article
Altered CB1 receptor and endocannabinoid levels precede motor symptom onset in a transgenic mouse model of Huntington's disease
MJ Dowie, HB Bradshaw, ML Howard, LFB Nicholson, RLM Faull, AJ Hannan, M Glass
Neuroscience | Published : 2009
Abstract
Huntington's disease (HD) is an inherited neurodegenerative disease characterised by cell dysfunction and death in the basal ganglia and cortex. Currently there are no effective pharmacological treatments available. Loss of cannabinoid CB1 receptor ligand binding in key brain regions is detected early in HD in human postmortem tissue [Glass M, Dragunow M, Faull RL (2000) The pattern of neurodegeneration in Huntington's disease: a comparative study of cannabinoid, dopamine, adenosine and GABA(A) receptor alterations in the human basal ganglia in Huntington's disease. Neuroscience 97:505-519]. In HD transgenic mice environmental enrichment upregulates the CB1 receptors and slows disease progre..
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Funding Acknowledgements
We thank L. Schwarcz for critical reading of this manuscript and J. Bullock for assistance with tissue processing. This work was supported by grants from the Neurological Foundation of New Zealand (M.G. and R.L.M.F.), the Australian National Health and Medical Research Council (A.J.H.) and a University of Auckland Health Research Doctoral Scholarship (M.J.D.).