NDLI: IGF-1 Intranasal Administration Rescues Huntington's Disease Phenotypes in YAC128 Mice

Content Provider	Springer Nature Link
Author	Lopes, Carla Ribeiro, Márcio Duarte, Ana I. Humbert, Sandrine Saudou, Frederic Pereira de Almeida, Luís Hayden, Michael Rego, A. Cristina
Copyright Year	2013
Abstract	Huntington's disease (HD) is an autosomal dominant disease caused by an expansion of CAG repeats in the gene encoding for huntingtin. Brain metabolic dysfunction and altered Akt signaling pathways have been associated with disease progression. Nevertheless, conflicting results persist regarding the role of insulin-like growth factor-1 (IGF-1)/Akt pathway in HD. While high plasma levels of IGF-1 correlated with cognitive decline in HD patients, other data showed protective effects of IGF-1 in HD striatal neurons and R6/2 mice. Thus, in the present study, we investigated motor phenotype, peripheral and central metabolic profile, and striatal and cortical signaling pathways in YAC128 mice subjected to intranasal administration of recombinant human IGF-1 (rhIGF-1) for 2 weeks, in order to promote IGF-1 delivery to the brain. We show that IGF-1 supplementation enhances IGF-1 cortical levels and improves motor activity and both peripheral and central metabolic abnormalities in YAC128 mice. Moreover, decreased Akt activation in HD mice brain was ameliorated following IGF-1 administration. Upregulation of Akt following rhIGF-1 treatment occurred concomitantly with increased phosphorylation of mutant huntingtin on Ser421. These data suggest that intranasal administration of rhIGF-1 ameliorates HD-associated glucose metabolic brain abnormalities and mice phenotype.
Starting Page	1126
Ending Page	1142
Page Count	17
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	49
Issue Number	3
e-ISSN	15591182
Language	English
Publisher	Springer US
Publisher Date	2013-12-18
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Huntington's disease IGF-1 YAC128 mice Huntingtin phosphorylation Energy metabolism Signaling pathways Animal behavior Neurosciences Neurobiology Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

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