ArticleScientific reports2021
Spatiotemporal analysis of soluble aggregates and autophagy markers in the R6/2 mouse model.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 11 citations in OpenAlex.
- Distinct molecular patterns in R6/2 HD mouse brain: Insights from spatiotemporal transcriptomics.Neuron · 2025Article
- Interventionally targeting somatic CAG expansions can be a rapid disease-modifying therapeutic avenue: Preclinical evidence.bioRxiv : the preprint server for biology · 2025Article
- Small molecule modulation of p75Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Restoration of Sleep and Circadian Behavior by Autophagy Modulation in Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- The tyrosine kinase inhibitor nilotinib targets the discoidin domain receptor DDR2 in calcific aortic valve stenosis.British journal of pharmacology · 2022Article
- Emerging Role of NLRP3 Inflammasome/Pyroptosis in Huntington's Disease.International journal of molecular sciences · 2022Review
- Reduction in PA28αβ activation in HD mouse brain correlates to increased mHTT aggregation in cell models.PloS one · 2022Article
- Current Status of Autophagy Enhancers in Metabolic Disorders and Other Diseases.Frontiers in cell and developmental biology · 2022Review
- New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021Review
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6 authors at 1 institution in 1 country.
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Abstract
Maintenance of cellular proteostasis is vital for post-mitotic cells like neurons to sustain normal physiological function and homeostasis, defects in which are established hallmarks of several age-related conditions like AD, PD, HD, and ALS. The Spatio-temporal accumulation of aggregated proteins in the form of inclusion bodies/plaques is one of the major characteristics of many neurodegenerative diseases, including Huntington's disease (HD). Toxic accumulation of HUNTINGTIN (HTT) aggregates in neurons bring about the aberrant phenotypes of HD, including severe motor dysfunction, dementia, and cognitive impairment at the organismal level, in an age-dependent manner. In several cellular and animal models, aggrephagy induction has been shown to clear aggregate-prone proteins like HTT and ameliorate disease pathology by conferring neuroprotection. In this study, we used the mouse model of HD, R6/2, to understand the pathogenicity of mHTT aggregates, primarily focusing on autophagy dysfunction. We report that basal autophagy is not altered in R6/2 mice, whilst being functional at a steady-state level in neurons. Moreover, we tested the efficacy of a known autophagy modulator, Nilotinib (Tasigna™), presently in clinical trials for PD, and HD, in curbing mHTT aggregate growth and their potential clearance, which was ineffective in both inducing autophagy and rescuing the pathological phenotypes in R6/2 mice.
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