Huntington’s Disease
Endocannabinoid-Specific Impairment in Synaptic Plasticity in Striatum of Huntington’s Disease Mouse Model
Marja D. Sepers, Amy Smith-Dijak, Jeff LeDue, Karolina Kolodziejczyk, Ken Mackie and Lynn A. Raymond (January 2018)
Huntington’s disease (HD) is an inherited neurodegenerative disease with no cure. Recent studies find impairment of the endocannabinoid system in animal models but the functional implication for synaptic plasticity in HD remains unclear. Sepers et al. show a selective deficit in synaptic plasticity mediated by the endocannabinoid anandamide, but not 2-arachidonoylglycerol in a mouse model of HD. The deficit is rescued by selectively elevating levels of 2-arachidonoylglycerol produced on-demand. This mechanism could be targeted in the development of future therapeutics for HD.
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Molecular insights into cortico-striatal miscommunications in Huntington’s disease
Matthew B Veldman, X WilliamYang (October 2017)
Mouse models of HD have been created that exhibit phenotypes partially recapitulating those in the patient, and specifically, cortico-striatal disconnectivity appears to be a shared pathogenic event shared by HD mouse models and patients. Molecular studies have begun to unveil converging molecular and cellular pathogenic mechanisms that may account for cortico-striatal miscommunication in various HD mouse models. Systems biological approaches help to illuminate synaptic molecular networks as a nexus for HD cortio-striatal pathogenesis, and may offer new candidate targets to modify the disease.
Important Notice
If you proceed to article you will be leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.
Exploring the Therapeutic Potential of the Endocannabinoid System in Huntington’s Disease
Joseph F Cheer (2017)
We have recently shown in the Q175 mouse model of HD that suppressed motivation – one of the earliest indicators of HD – is associated with compromised dopaminergic signaling and network dynamics in the nucleus accumbens (NAc). We will discuss how pharmacological elevation of endocannabinoid levels in Q175 mice rescues compromised neurobiological markers and ameliorates motivational deficits. Our findings indicate that modulating NAc abnormalities with endocannabinoid-based therapies may be beneficial in treating the prodromal psychiatric deficits of HD.
Important Notice
If you proceed to article you will be leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.