ArticleInternational journal of molecular sciences2018
GLP-1 Analogue Liraglutide Attenuates Mutant Huntingtin-Induced Neurotoxicity by Restoration of Neuronal Insulin Signaling.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- The promise of GLP-1 receptor agonists for neurodegenerative diseases.The Journal of clinical investigation · 2026Review
- GLP-1 Receptor Agonists in Neurological Disorders: From Mechanisms to Clinical Translation.Drug design, development and therapy · 2026Review
- Glucagon-like peptide-1 receptor agonists in movement disorders: From Parkinson's disease to the broader spectrum - Mechanisms, evidence, and future directions.Clinical parkinsonism & related disorders · 2026Review
- GLP-1 and the Degenerating Brain: Exploring Mechanistic Insights and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Glucagon-Like Peptide-1 Receptor Agonists in Neurodegenerative Diseases: A Comprehensive Review.Cureus · 2025Review
- Human Glucose Transporters in Health and Selected Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Hormonal modulation, mitochondria and Alzheimer's prevention: the role of GLP-1 agonists and estrogens.Frontiers in molecular biosciences · 2025Review
- The Beneficial Effects of GLP-1 Receptor Agonists Other than Their Anti-Diabetic and Anti-Obesity Properties.Medicina (Kaunas, Lithuania) · 2024Review
- Review
- Glp-1 Mimetics and Autophagy in Diabetic Milieu: State-of-the-Art.Current diabetes reviews · 2024Review
- Glucagon-like peptide-1 receptor agonists in neoplastic diseases.Frontiers in endocrinology · 2024Review
- Review
- Mechanistic Insights and Potential Therapeutic Approaches in PolyQ Diseases via Autophagy.Biomedicines · 2023Review
- The interplay between oxidative stress and autophagy: focus on the development of neurological diseases.Behavioral and brain functions : BBF · 2022Review
- Exploring the Role of Autophagy Dysfunction in Neurodegenerative Disorders.Molecular neurobiology · 2021Review
- miR-302 Attenuates Mutant Huntingtin-Induced Cytotoxicity through Restoration of Autophagy and Insulin Sensitivity.International journal of molecular sciences · 2021Article
- Peganum harmala enhanced GLP-1 and restored insulin signaling to alleviate AlClScientific reports · 2021Article
- The impact of proteostasis dysfunction secondary to environmental and genetic causes on neurodegenerative diseases progression and potential therapeutic intervention.Environmental science and pollution research international · 2020Review
- Gut microbiome: An intermediary to neurotoxicity.Neurotoxicology · 2019Review
- Glucagon-like peptide 1 (GLP-1).Molecular metabolism · 2019 · on this mapReview
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a progressive and fatal neurodegenerative disease caused by CAG repeat expansion in the coding region of huntingtin (HTT) protein. The accumulation of mutant HTT (mHTT) contributes to neurotoxicity by causing autophagy defects and oxidative stress that ultimately lead to neuronal death. Interestingly, epidemiologic studies have demonstrated that the prevalence of type-2 diabetes, a metabolic disease mainly caused by defective insulin signaling, is higher in patients with HD than in healthy controls. Although the precise mechanisms of mHTT-mediated toxicity remain unclear, the blockade of brain insulin signaling may initiate or exacerbate mHTT-induced neurodegeneration. In this study, we used an in vitro HD model to investigate whether neuronal insulin signaling is involved in mHTT-mediated neurotoxicity. Our results demonstrated that mHTT overexpression significantly impairs insulin signaling and causes apoptosis in neuronal cells. However, treatment with liraglutide, a GLP-1 analogue, markedly restores insulin sensitivity and enhances cell viability. This neuroprotective effect may be attributed to the contribution of the upregulated expression of genes associated with endogenous antioxidant pathways to oxidative stress reduction. In addition, liraglutide stimulates autophagy through AMPK activation, which attenuates the accumulation of HTT aggregates within neuronal cells. Our findings collectively suggest that liraglutide can rescue impaired insulin signaling caused by mHTT and that GLP-1 may potentially reduce mHTT-induced neurotoxicity in the pathogenesis of HD.
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Registered trials
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