ArticleBio-protocol2021
A Parkinson's Disease-relevant Mitochondrial and Neuronal Morphology High-throughput Screening Assay in LUHMES Cells.
Article in Bio-protocol, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Differentiated LUHMES Cells as a Model to Investigate Neurotropic Arboviruses and Evaluate Host-Directed Therapeutics.Microorganisms · 2026Article
- From mice to clinical relevance: humanizing neuroscience with human-based model systems.Frontiers in cellular neuroscience · 2026Review
- Research models to study lewy body dementia.Molecular neurodegeneration · 2025Review
- Disruption of Mitochondrial-associated ER membranes by HIV-1 tat protein contributes to premature brain aging.CNS neuroscience & therapeutics · 2023Article
- Identification of DOT1L inhibitor in a screen for factors that promote dopaminergic neuron survival.Frontiers in aging neuroscience · 2022Article
- Astrocytic C-X-C motif chemokine ligand-1 mediates β-amyloid-induced synaptotoxicity.Journal of neuroinflammation · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease is a devastating neurodegenerative disorder affecting 2-3% of the population over 65 years of age. There is currently no disease-modifying treatment. One of the predominant pathological features of Parkinson's disease is mitochondrial dysfunction, and much work has aimed to identify therapeutic compounds which can restore the disrupted mitochondrial physiology. However, modelling mitochondrial dysfunction in a disease-relevant model, suitable for screening large compound libraries for ameliorative effects, represents a considerable challenge. Primary patient derived cells, SHSY-5Y cells and
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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.