Please use this identifier to cite or link to this item:
https://doi.org/10.3389/fncel.2018.00413
DC Field | Value | |
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dc.title | Patient-derived induced pluripotent stem cells and organoids for modeling alpha synuclein propagation in parkinson's disease | |
dc.contributor.author | Koh, Y.H | |
dc.contributor.author | Tan, L.Y | |
dc.contributor.author | Ng, S.-Y | |
dc.date.accessioned | 2020-09-09T09:51:58Z | |
dc.date.available | 2020-09-09T09:51:58Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Koh, Y.H, Tan, L.Y, Ng, S.-Y (2018). Patient-derived induced pluripotent stem cells and organoids for modeling alpha synuclein propagation in parkinson's disease. Frontiers in Cellular Neuroscience 12 : 413. ScholarBank@NUS Repository. https://doi.org/10.3389/fncel.2018.00413 | |
dc.identifier.issn | 1662-5102 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/175357 | |
dc.description.abstract | Parkinson's disease (PD) is an age-associated, progressive neurodegenerative disorder characterized by motor impairment and in some cases cognitive decline. Central to the disease pathogenesis of PD is a small, presynaptic neuronal protein known as alpha synuclein (a-syn), which tends to accumulate and aggregate in PD brains as Lewy bodies or Lewy neurites. Numerous in vitro and in vivo studies confirm that a-syn aggregates can be propagated from diseased to healthy cells, and it has been suggested that preventing the spread of pathogenic a-syn species can slow PD progression. In this review, we summarize the works of recent literature elucidating mechanisms of a-syn propagation, and discussed the advantages in using patient-derived induced pluripotent stem cells (iPSCs) and/or induced neurons to study a-syn transmission. © 2018 Koh, Tan and Ng. | |
dc.source | Unpaywall 20200831 | |
dc.subject | alpha synuclein | |
dc.subject | dorsomorphin | |
dc.subject | transcription factor Sox6 | |
dc.subject | astrocyte | |
dc.subject | brain electrophysiology | |
dc.subject | brain function | |
dc.subject | cell activation | |
dc.subject | cell differentiation | |
dc.subject | cell survival | |
dc.subject | disease exacerbation | |
dc.subject | endocytosis | |
dc.subject | exocytosis | |
dc.subject | gene delivery system | |
dc.subject | gene overexpression | |
dc.subject | human | |
dc.subject | internalization | |
dc.subject | microglia | |
dc.subject | molecular pathology | |
dc.subject | neurotransmission | |
dc.subject | nonhuman | |
dc.subject | oligodendroglia | |
dc.subject | organoid | |
dc.subject | Parkinson disease | |
dc.subject | pathogenesis | |
dc.subject | pluripotent stem cell | |
dc.subject | Short Survey | |
dc.subject | tumor microenvironment | |
dc.type | Others | |
dc.contributor.department | PHYSIOLOGY | |
dc.description.doi | 10.3389/fncel.2018.00413 | |
dc.description.sourcetitle | Frontiers in Cellular Neuroscience | |
dc.description.volume | 12 | |
dc.description.page | 413 | |
dc.published.state | Published | |
Appears in Collections: | Staff Publications Elements |
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