ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Pharmacological and genetic reversal of age-dependent cognitive deficits attributable to decreased presenilin function.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- TDP-43 impairs sleep inScience advances · 2024Article
- Lipophorin receptors genetically modulate neurodegeneration caused by reduction of Psn expression in the aging Drosophila brain.Genetics · 2024Article
- Biological aging of two innate behaviors of Drosophila melanogaster: Escape climbing versus courtship learning and memory.PloS one · 2024Article
- Review
- Fragile X and APP: a Decade in Review, a Vision for the Future.Molecular neurobiology · 2019Review
- Presenilin-1 Delta E9 Mutant Induces STIM1-Driven Store-Operated Calcium Channel Hyperactivation in Hippocampal Neurons.Molecular neurobiology · 2018Article
- Repurposing Proteostasis-Modifying Drugs to Prevent or Treat Age-Related Dementia: A Systematic Review.Frontiers in physiology · 2018Article
- Article
- Enhanced sleep reverses memory deficits and underlying pathology in Drosophila models of Alzheimer's disease.Neurobiology of sleep and circadian rhythms · 2017Article
- Six psychotropics for pre-symptomatic & early Alzheimer's (MCI), Parkinson's, and Huntington's disease modification.Neural regeneration research · 2016Review
- Candidate genes for individual recognition in Polistes fuscatus paper wasps.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2016Article
- Multiple Drug Treatments That Increase cAMP Signaling Restore Long-Term Memory and Aberrant Signaling in Fragile X Syndrome Models.Frontiers in behavioral neuroscience · 2016Article
- Sleep restores behavioral plasticity to Drosophila mutants.Current biology : CB · 2015Article
- 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
- Article
- Lipid rafts serve as signaling platforms for mGlu1 receptor-mediated calcium signaling in association with caveolin.Molecular brain · 2014Article
- The Drosophila DmGluRA is required for social interaction and memory.Frontiers in pharmacology · 2013Article
- Preclinical non-human models to combat dementia.Annals of neurosciences · 2013Review
- Group 1 metabotropic glutamate receptor function and its regulation of learning and memory in the aging brain.Frontiers in pharmacology · 2012Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the leading cause of cognitive loss and neurodegeneration in the developed world. Although its genetic and environmental causes are not generally known, familial forms of the disease (FAD) are attributable to mutations in a single copy of the Presenilin (PS) and amyloid precursor protein genes. The dominant inheritance pattern of FAD indicates that it may be attributable to gain or change of function mutations. Studies of FAD-linked forms of presenilin (psn) in model organisms, however, indicate that they are loss of function, leading to the possibility that a reduction in PS activity might contribute to FAD and that proper psn levels are important for maintaining normal cognition throughout life. To explore this issue further, we have tested the effect of reducing psn activity during aging in Drosophila melanogaster males. We have found that flies in which the dosage of psn function is reduced by 50% display age-onset impairments in learning and memory. Treatment with metabotropic glutamate receptor (mGluR) antagonists or lithium during the aging process prevented the onset of these deficits, and treatment of aged flies reversed the age-dependent deficits. Genetic reduction of Drosophila metabotropic glutamate receptor (DmGluRA), the inositol trisphosphate receptor (InsP(3)R), or inositol polyphosphate 1-phosphatase also prevented these age-onset cognitive deficits. These findings suggest that reduced psn activity may contribute to the age-onset cognitive loss observed with FAD. They also indicate that enhanced mGluR signaling and calcium release regulated by InsP(3)R as underlying causes of the age-dependent cognitive phenotypes observed when psn activity is reduced.
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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.