ArticleNeuroscience2015
Altered iPSC-derived neurons' sodium channel properties in subjects with Monge's disease.
Article in Neuroscience, 2015. 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Chronic high-altitude exposure and intracerebral hemorrhage: A novel perspective from the vascular-immune-neuronal network.Neuroprotection (Chichester, England) · 2026Review
- Long noncoding RNA HIKER regulates erythropoiesis in Monge's disease via CSNK2B.The Journal of clinical investigation · 2023Article
- ARID1B, a molecular suppressor of erythropoiesis, is essential for the prevention of Monge's disease.Experimental & molecular medicine · 2022Article
- Protective role of estrogen against excessive erythrocytosis in Monge's disease.Experimental & molecular medicine · 2021Article
- Neuroprotective Role of Akt in Hypoxia Adaptation in Andeans.Frontiers in neuroscience · 2020Article
- Mitochondrial dysfunction in iPSC-derived neurons of subjects with chronic mountain sickness.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Intracellular pH Regulation in iPSCs-derived Astrocytes from Subjects with Chronic Mountain Sickness.Neuroscience · 2018Article
- The translational potential of human induced pluripotent stem cells for clinical neurology : The translational potential of hiPSCs in neurology.Cell biology and toxicology · 2017Review
- The NaNeuroscience · 2016Article
- Senp1 drives hypoxia-induced polycythemia via GATA1 and Bcl-xL in subjects with Monge's disease.The Journal of experimental medicine · 2016Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Monge's disease, also known as chronic mountain sickness (CMS), is a disease that potentially threatens more than 140 million highlanders during extended time living at high altitudes (over 2500m). The prevalence of CMS in Andeans is about 15-20%, suggesting that the majority of highlanders (non-CMS) are rather healthy at high altitudes; however, CMS subjects experience severe hypoxemia, erythrocytosis and many neurologic manifestations including migraine, headache, mental fatigue, confusion, and memory loss. The underlying mechanisms of CMS neuropathology are not well understood and no ideal treatment is available to prevent or cure CMS, except for phlebotomy. In the current study, we reprogrammed fibroblast cells from both CMS and non-CMS subjects' skin biopsies into the induced pluripotent stem cells (iPSCs), then differentiated into neurons and compared their neuronal properties. We discovered that CMS neurons were much less excitable (higher rheobase) than non-CMS neurons. This decreased excitability was not caused by differences in passive neuronal properties, but instead by a significantly lowered Na(+) channel current density and by a shift of the voltage-conductance curve in the depolarization direction. Our findings provide, for the first time, evidence of a neuronal abnormality in CMS subjects as compared to non-CMS subjects, hoping that such studies can pave the way to a better understanding of the neuropathology in CMS.
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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 OpenQuestion graph.