ArticleFrontiers in pharmacology2021
Liraglutide Improves Cognitive and Neuronal Function in 3-NP Rat Model of Huntington's Disease.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 43 citations in OpenAlex.
- The promise of GLP-1 receptor agonists for neurodegenerative diseases.The Journal of clinical investigation · 2026Review
- GLP-1 Signalling as a Therapeutic Avenue in Parkinson's Disease: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Bibliometric analysis and core target identification of network pharmacology on neuroinflammation in central nervous system disorders: Trends, collaborations, and future directions.Neuroprotection (Chichester, England) · 2025Review
- GLP-1 and the Degenerating Brain: Exploring Mechanistic Insights and Therapeutic Potential.International journal of molecular sciences · 2025Review
- The Intricate Relationship of Trk Receptors in Brain Diseases and Disorders.Molecular neurobiology · 2025Review
- Glucagon-Like Peptide-1 Receptor Agonists in Neurodegenerative Diseases: A Comprehensive Review.Cureus · 2025Review
- Ferulic acid mitigates 3-Nitropropionic acid-induced Huntington's disease via modulation of Nrf2/HO-1, TLR4/NF-κB, and SIRT1/p53 signaling pathways.Frontiers in pharmacology · 2025Article
- Flavonoids and phenolic compounds: a promising avenue for neurodegenerative disease therapy.Turkish journal of biology = Turk biyoloji dergisi · 2025Review
- Role of Liraglutide in weight management and reproductive health in women with obesity and PCOS- A critical review of the evidence.F1000Research · 2025Review
- The Beneficial Effects of GLP-1 Receptor Agonists Other than Their Anti-Diabetic and Anti-Obesity Properties.Medicina (Kaunas, Lithuania) · 2024Review
- Mitochondrial targeted antioxidants as potential therapy for huntington's disease.Pharmacological reports : PR · 2024Review
- Liraglutide versus pramlintide in protecting against cognitive function impairment through affecting PI3K/AKT/GSK-3β/TTBK1 pathway and decreasing Tau hyperphosphorylation in high-fat diet- streptozocin rat model.Pflugers Archiv : European journal of physiology · 2024Article
- Azilsartan Attenuates 3-Nitropropinoic Acid-Induced Neurotoxicity in Rats: The Role of IĸB/NF-ĸB and KEAP1/Nrf2 Signaling Pathways.Neurochemical research · 2024Article
- Article
- Review
- An Overview of the Pathophysiological Mechanisms of 3-Nitropropionic Acid (3-NPA) as a Neurotoxin in a Huntington's Disease Model and Its Relevance to Drug Discovery and Development.Neurochemical research · 2023Review
- Targeting redox imbalance in neurodegeneration: characterizing the role of GLP-1 receptor agonists.Theranostics · 2023Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is an autosomal dominant inherited neurodegenerative disease characterized by progressive motor, psychiatric, and cognitive abnormalities. The antidiabetic drug liraglutide possesses a neuroprotective potential against several neurodegenerative disorders; however, its role in Huntington's disease (HD) and the possible mechanisms/trajectories remain elusive, which is the aim of this work. Liraglutide (200 μg/kg, s.c) was administered to rats intoxicated with 3-nitropropionic acid (3-NP) for 4 weeks post HD model induction. Liraglutide abated the 3-NP-induced neurobehavioral deficits (open field and elevated plus maze tests) and histopathological changes. Liraglutide downregulated the striatal mRNA expression of HSP 27, PBR, and GFAP, while it upregulated that of DARPP32. On the molecular level, liraglutide enhanced striatal miR-130a gene expression and TrKB protein expression and its ligand BDNF, while it reduced the striatal protein content and mRNA expression of the death receptors sortilin and p75NTR, respectively. It enhanced the neuroprotective molecules cAMP, p-PI3K, p-Akt, and p-CREB, besides modulating the
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