ArticleMolecular neurobiology2014
IGF-1 intranasal administration rescues Huntington's disease phenotypes in YAC128 mice.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 70 citations in OpenAlex.
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- Application of Neurotrophic Factors as a Therapeutic Approach for Neurodegenerative Diseases.Experimental neurobiology · 2025Review
- Downregulation of Pten Improves Huntington's Disease Phenotype by Reducing Htt Aggregates and Cell Death.Molecular neurobiology · 2025Article
- Insulin-Like Growth Factor Signaling in Alzheimer's Disease: Pathophysiology and Therapeutic Strategies.Molecular neurobiology · 2025Review
- Intranasal long R3 insulin-like growth factor-1 treatment promotes amyloid plaque remodeling in cerebral cortex but fails to preserve cognitive function in male 5XFAD mice.Journal of Alzheimer's disease : JAD · 2025Article
- Review
- A Historical Review of Brain Drug Delivery.Pharmaceutics · 2022Review
- Review
- Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021Review
- New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021Review
- Physical Exercise-Induced Myokines in Neurodegenerative Diseases.International journal of molecular sciences · 2021Review
- Cell-penetrating, antioxidant SELENOT mimetic protects dopaminergic neurons and ameliorates motor dysfunction in Parkinson's disease animal models.Redox biology · 2021Article
- The Effects of Selective Inhibition of Histone Deacetylase 1 and 3 in Huntington's Disease Mice.Frontiers in molecular neuroscience · 2021Article
- Huntington's disease genotype suppresses global manganese-responsive processes in pre-manifest and manifest YAC128 mice.Metallomics : integrated biometal science · 2020Article
- Manganese Acts upon Insulin/IGF Receptors to Phosphorylate AKT and Increase Glucose Uptake in Huntington's Disease Cells.Molecular neurobiology · 2020Article
- Progerin-Induced Transcriptional Changes in Huntington's Disease Human Pluripotent Stem Cell-Derived Neurons.Molecular neurobiology · 2020Article
- On the Right Track to Treat Movement Disorders: Promising Therapeutic Approaches for Parkinson's and Huntington's Disease.Frontiers in aging neuroscience · 2020Review
- Biological Aging and the Cellular Pathogenesis of Huntington's Disease.Journal of Huntington's disease · 2020Review
- Loss of insulin-like growth factor-1 signaling in astrocytes disrupts glutamate handling.Journal of neurochemistry · 2019Article
- Central IGF-1 protects against features of cognitive and sensorimotor decline with aging in male mice.GeroScience · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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