ArticlePloS one2015
Reduction in subventricular zone-derived olfactory bulb neurogenesis in a rat model of Huntington's disease is accompanied by striatal invasion of neuroblasts.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 47 citations in OpenAlex.
- Olfactory impairment in Huntington's disease: A systematic review and meta-analysis.Neuroscience applied · 2026Article
- Exploring huntington's disease from a neurodevelopmental perspective.International journal of biological sciences · 2026Review
- Astrocyte-neuron combined targeting for CYP46A1 gene therapy in Huntington's disease.Acta neuropathologica communications · 2025Article
- Review
- Migratory Response of Cells in Neurogenic Niches to Neuronal Death: The Onset of Harmonic Repair?International journal of molecular sciences · 2023Review
- COVID-19 causes neuronal degeneration and reduces neurogenesis in human hippocampus.Apoptosis : an international journal on programmed cell death · 2022Article
- Article
- COVID-19 and Parkinson's disease: Defects in neurogenesis as the potential cause of olfactory system impairments and anosmia.Journal of chemical neuroanatomy · 2021Review
- Reconditioning the Neurogenic Niche of Adult Non-human Primates by Antisense Oligonucleotide-Mediated Attenuation of TGFβ Signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Article
- Tissue Engineering and Biomaterial Strategies to Elicit Endogenous Neuronal Replacement in the Brain.Frontiers in neurology · 2020Review
- MicroalgaeFrontiers in cell and developmental biology · 2020Article
- Non-motor symptoms in Huntington's disease: a comparative study with Parkinson's disease.Journal of neurology · 2019Article
- Article
- Protein Kinase C: Targets to Regenerate Brain Injuries?Frontiers in cell and developmental biology · 2019Article
- Early postnatal behavioral, cellular, and molecular changes in models of Huntington disease are reversible by HDAC inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Neuroplasticity, limbic neuroblastosis and neuro-regenerative disorders.Neural regeneration research · 2018Review
- Microglial involvement in the development of olfactory dysfunction.Journal of veterinary science · 2018Review
- Regenerative Approaches in Huntington's Disease: From Mechanistic Insights to Therapeutic Protocols.Frontiers in neuroscience · 2018Review
- Reactive Neuroblastosis in Huntington's Disease: A Putative Therapeutic Target for Striatal Regeneration in the Adult Brain.Frontiers in cellular neuroscience · 2018Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is an inherited progressive neurodegenerative disorder caused by an expanded CAG repeat in exon 1 of the huntingtin gene (HTT). The primary neuropathology of HD has been attributed to the preferential degeneration of medium spiny neurons (MSN) in the striatum. Reports on striatal neurogenesis have been a subject of debate; nevertheless, it should be considered as an endogenous attempt to repair the brain. The subventricular zone (SVZ) might offer a close-by region to supply the degenerated striatum with new cells. Previously, we have demonstrated that R6/2 mice, a widely used preclinical model representing an early onset HD, showed reduced olfactory bulb (OB) neurogenesis but induced striatal migration of neuroblasts without affecting the proliferation of neural progenitor cell (NPCs) in the SVZ. The present study revisits these findings, using a clinically more relevant transgenic rat model of late onset HD (tgHD rats) carrying the human HTT gene with 51 CAG repeats and mimicking many of the neuropathological features of HD seen in patients. We demonstrate that cell proliferation is reduced in the SVZ and OB of tgHD rats compared to WT rats. In the OB of tgHD rats, although cell survival was reduced, the frequency of neuronal differentiation was not altered in the granule cell layer (GCL) compared to the WT rats. However, an increased frequency of dopamenergic neuronal differentiation was noticed in the glomerular layer (GLOM) of tgHD rats. Besides this, we observed a selective proliferation of neuroblasts in the adjacent striatum of tgHD rats. There was no evidence for neuronal maturation and survival of these striatal neuroblasts. Therefore, the functional role of these invading neuroblasts still needs to be determined, but they might offer an endogenous alternative for stem or neuronal cell transplantation strategies.
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