ReviewCurrent pharmaceutical design2012
Drosophila models of proteinopathies: the little fly that could.
Review in Current pharmaceutical design, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 51 citations in OpenAlex.
- Signaling interactions among neurons impact cell fitness and death in Alzheimer's disease.Neural regeneration research · 2023Article
- Intrinsic determinants of prion protein neurotoxicity inFrontiers in molecular neuroscience · 2023Review
- Ayurvedic formulations Guduchi and Madhuyashti triggers JNK signaling mediated immune response and adversely affects Huntington phenotype.BMC complementary medicine and therapies · 2022Article
- Modifier pathways in polyglutamine (PolyQ) diseases: from genetic screens to drug targets.Cellular and molecular life sciences : CMLS · 2022Review
- Nicotine Has a Therapeutic Window of Effectiveness in aParkinson's disease · 2022Article
- Activity-dependent release of phosphorylated human tau from Drosophila neurons in primary culture.The Journal of biological chemistry · 2021Article
- Article
- Role of Tau Protein in Remodeling of Circadian Neuronal Circuits and Sleep.Frontiers in aging neuroscience · 2019Article
- A soy protein Lunasin can ameliorate amyloid-beta 42 mediated neurodegeneration in Drosophila eye.Scientific reports · 2018Article
- High and Low Levels of an NTRK2-Driven Genetic Profile Affect Motor- and Cognition-Associated Frontal Gray Matter in Prodromal Huntington's Disease.Brain sciences · 2018Article
- Drosophila models of prionopathies: insight into prion protein function, transmission, and neurotoxicity.Current opinion in genetics & development · 2017Review
- MicroRNA function in Drosophila memory formation.Current opinion in neurobiology · 2017Review
- Holdase activity of secreted Hsp70 masks amyloid-β42 neurotoxicity in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The contribution of mutant GBA to the development of Parkinson disease in Drosophila.Human molecular genetics · 2016Article
- Deletion of endogenous Tau proteins is not detrimental in Drosophila.Scientific reports · 2016Article
- Modeling the complex pathology of Alzheimer's disease in Drosophila.Experimental neurology · 2015Review
- Transmission, Development, and Plasticity of Synapses.Genetics · 2015Review
- A fruitful endeavor: modeling ALS in the fruit fly.Brain research · 2015Review
- Drosophila Eye Model to Study Neuroprotective Role of CREB Binding Protein (CBP) in Alzheimer's Disease.PloS one · 2015Article
- Using membrane-targeted green fluorescent protein to monitor neurotoxic protein-dependent degeneration of Drosophila eyes.Journal of neuroscience research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's, Parkinson's, and Huntington's disease are complex neurodegenerative conditions with high prevalence characterized by protein misfolding and deposition in the brain. Considerable progress has been made in the last two decades in identifying the genes and proteins responsible for several human 'proteinopathies'. A wide variety of wild type and mutant proteins associated with neurodegenerative conditions are structurally unstable, misfolded, and acquire conformations rich in ß-sheets (ß-state). These conformers form highly toxic self-assemblies that kill the neurons in stereotypical patterns. Unfortunately, the detailed understanding of the molecular and cellular perturbations caused by these proteins has not produced a single disease-modifying therapy. More than a decade ago, several groups demonstrated that human proteinopathies reproduce critical features of the disease in transgenic flies, including protein mis-folding, aggregation, and neurotoxicity. These initial reports led to an explosion of research that has contributed to a better understanding of the molecular mechanisms regulating conformational dynamics and neurotoxic cascades. To remain relevant in this competitive environment, Drosophila models will need to expand their flexible, innovative, and multidisciplinary approaches to find new discoveries and translational applications.
Indexed as
Identifiers
What OpenQuestion holds
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.