ArticleBiogerontology2010
Age-dependent cognitive impairment in a Drosophila fragile X model and its pharmacological rescue.
Article in Biogerontology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 61 citations in OpenAlex.
- An experimentally validated approach to automated biological evidence generation in drug discovery using knowledge graphs.Nature communications · 2024Article
- From wings to whiskers to stem cells: why every model matters in fragile X syndrome research.Journal of neurodevelopmental disorders · 2024Review
- Article
- Effects of lithium on aggression in Drosophila.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Review
- Review
- TestingFrontiers in molecular neuroscience · 2021Article
- Autism Spectrum Disorder-Related Syndromes: Modeling withInternational journal of molecular sciences · 2019Review
- Molecular Biomarkers in Fragile X Syndrome.Brain sciences · 2019Review
- Dissecting the Genetics of Autism Spectrum Disorders: AFrontiers in physiology · 2019Review
- Review
- Presenilin-1 Delta E9 Mutant Induces STIM1-Driven Store-Operated Calcium Channel Hyperactivation in Hippocampal Neurons.Molecular neurobiology · 2018Article
- Modeling Fragile X Syndrome inFrontiers in molecular neuroscience · 2018Review
- Fragile X Mental Retardation Protein Requirements in Activity-Dependent Critical Period Neural Circuit Refinement.Current biology : CB · 2017Article
- Fragile X Mental Retardation Protein Regulates Activity-Dependent Membrane Trafficking andFrontiers in molecular neuroscience · 2017Review
- Multiple Drug Treatments That Increase cAMP Signaling Restore Long-Term Memory and Aberrant Signaling in Fragile X Syndrome Models.Frontiers in behavioral neuroscience · 2016Article
- Deciphering discord: How Drosophila research has enhanced our understanding of the importance of FMRP in different spatial and temporal contexts.Experimental neurology · 2015Review
- Therapeutic Strategies in Fragile X Syndrome: From Bench to Bedside and Back.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Review
- PDE-4 inhibition rescues aberrant synaptic plasticity in Drosophila and mouse models of fragile X syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Emerging pharmacologic treatment options for fragile X syndrome.The application of clinical genetics · 2015Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Fragile X syndrome afflicts 1 in 2,500 individuals and is the leading heritable cause of mental retardation worldwide. The overriding clinical manifestation of this disease is mild to severe cognitive impairment. Age-dependent cognitive decline has been identified in Fragile X patients, although it has not been fully characterized nor examined in animal models. A Drosophila model of this disease has been shown to display phenotypes bearing similarity to Fragile X symptoms. Most notably, we previously identified naive courtship and memory deficits in young adults with this model that appear to be due to enhanced metabotropic glutamate receptor (mGluR) signaling. Herein we have examined age-related cognitive decline in the Drosophila Fragile X model and found an age-dependent loss of learning during training. We demonstrate that treatment with mGluR antagonists or lithium can prevent this age-dependent cognitive impairment. We also show that treatment with mGluR antagonists or lithium during development alone displays differential efficacy in its ability to rescue naive courtship, learning during training and memory in aged flies. Furthermore, we show that continuous treatment during aging effectively rescues all of these phenotypes. These results indicate that the Drosophila model recapitulates the age-dependent cognitive decline observed in humans. This places Fragile X in a category with several other diseases that result in age-dependent cognitive decline. This demonstrates a role for the Drosophila Fragile X Mental Retardation Protein (dFMR1) in neuronal physiology with regard to cognition during the aging process. Our results indicate that misregulation of mGluR activity may be causative of this age onset decline and strengthens the possibility that mGluR antagonists and lithium may be potential pharmacologic compounds for counteracting several Fragile X symptoms.
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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.