ArticleJournal of Huntington's disease2019
Characterization of Neurodevelopmental Abnormalities in iPSC-Derived Striatal Cultures from Patients with Huntington's Disease.
Article in Journal of Huntington's disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Transcriptional vulnerabilities of striatal neurons in human and rodent models of Huntington's disease.Nature communications · 2023Article
- Patient-Specific iPSCs-Based Models of Neurodegenerative Diseases: Focus on Aberrant Calcium Signaling.International journal of molecular sciences · 2022Review
- Cerebral Organoids and Antisense Oligonucleotide Therapeutics: Challenges and Opportunities.Frontiers in molecular neuroscience · 2022Review
- Huntington's disease iPSC models-using human patient cells to understand the pathology caused by expanded CAG repeats.Faculty reviews · 2022Review
- Review
- Molecular Components of Store-Operated Calcium Channels in the Regulation of Neural Stem Cell Physiology, Neurogenesis, and the Pathology of Huntington's Disease.Frontiers in cell and developmental biology · 2021Review
- Neural stem cells derived from the developing forebrain of YAC128 mice exhibit pathological features of Huntington's disease.Cell proliferation · 2020Article
- Aberrant Development Corrected in Adult-Onset Huntington's Disease iPSC-Derived Neuronal Cultures via WNT Signaling Modulation.Stem cell reports · 2020Article
- Multi-lineage Human iPSC-Derived Platforms for Disease Modeling and Drug Discovery.Cell stem cell · 2020Review
- Biological Aging and the Cellular Pathogenesis of Huntington's Disease.Journal of Huntington's disease · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuntington's disease (HD) is an inherited neurodegenerative disease and is characterized by atrophy of certain regions of the brain in a progressive manner. HD patients experience behavioral changes and uncontrolled movements which can be primarily attributed to the atrophy of striatal neurons. Previous publications describe the models of the HD striatum using induced pluripotent stem cells (iPSCs) derived from HD patients with a juvenile onset (JHD). In this model, the JHD iPSC-derived striatal cultures had altered neurodevelopment and contained a high number of nestin expressing progenitor cells at 42 days of differentiation.
objectiveTo further characterize the altered neurodevelopmental phenotype and evaluate potential phenotypic reversal.
methodsDifferentiation of human iPSCs towards striatal fate and characterization by means of immunocytochemistry and stereological quantification.
resultsHere this study demonstrates a distinct delay in the differentiation of the JHD neural progenitor population. However, reduction of the JHD aberrant progenitor populations can be accomplished either by targeting the canonical Notch signaling pathway or by treatment with HTT antisense oligonucleotides (ASOs).
conclusionsIn summary, this data is postulated to reflect a potential overall developmental delay in JHD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.