ArticleBiological psychiatry2019
RPS23RG1 Is Required for Synaptic Integrity and Rescues Alzheimer's Disease-Associated Cognitive Deficits.
Article in Biological psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
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- The autocrine motility factor receptor delays the pathological progression of Alzheimer's disease via regulating the ubiquitination-mediated degradation of APP.Alzheimer's research & therapy · 2025Article
- Mdga2 deficiency leads to an aberrant activation of BDNF/TrkB signaling that underlies autism-relevant synaptic and behavioral changes in mice.PLoS biology · 2025Article
- Electrophysiology-based screening identifies neuronal HtrA serine peptidase 2 (HTRA2) as a synaptic plasticity regulator participating in tauopathy.Translational psychiatry · 2025Article
- RPS23RG1 inhibits SORT1-mediated lysosomal degradation of MDGA2 to protect against autism.Theranostics · 2025Article
- Delivering synaptic protein mRNAs via extracellular vesicles ameliorates cognitive impairment in a mouse model of Alzheimer's disease.BMC medicine · 2024Article
- Altered synaptic currents, mitophagy, mitochondrial dynamics in Alzheimer's disease models and therapeutic potential of Dengzhan Shengmai capsules intervention.Journal of pharmaceutical analysis · 2024Article
- Tau reduction attenuates autism-like features in Fmr1 knockout mice.Molecular autism · 2023Article
- Gene therapy using human FMRP isoforms driven by the humanMolecular therapy. Methods & clinical development · 2022Article
- Phenazopyridine promotes RPS23RG1/Rps23rg1 transcription and ameliorates Alzheimer-associated phenotypes in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
- Pedigree-based study to identify GOLGB1 as a risk gene for bipolar disorder.Translational psychiatry · 2022Article
- MicroglialThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Identification of Differential Genes of DNA Methylation Associated With Alzheimer's Disease Based on Integrated Bioinformatics and Its Diagnostic Significance.Frontiers in aging neuroscience · 2022Article
- Resilience in Long-Term Viral Infection: Genetic Determinants and Interactions.International journal of molecular sciences · 2021Article
- Hippocampal CysLT1R overexpression or activation accelerates memory deficits, synaptic dysfunction, and amyloidogenesis in young APP/PS1 transgenic mice.Annals of translational medicine · 2021Article
- RPS23RG1 modulates tau phosphorylation and axon outgrowth through regulating p35 proteasomal degradation.Cell death and differentiation · 2021Article
- RAB39B Deficiency Impairs Learning and Memory Partially Through Compromising Autophagy.Frontiers in cell and developmental biology · 2020Article
- Overexpression of HumanFrontiers in cell and developmental biology · 2020Article
- microRNA-34a (miRNA-34a) Mediated Down-Regulation of the Post-synaptic Cytoskeletal Element SHANK3 in Sporadic Alzheimer's Disease (AD).Frontiers in neurology · 2019Article
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Authors and funding
24 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAlthough synaptic impairment is a prerequisite to cognitive deficiencies in Alzheimer's disease (AD), mechanisms underlying the dysregulation of essential synaptic scaffolding components and their integrity remain elusive. RPS23RG1 is a newly identified protein implicated in AD. However, the physiological function of RPS23RG1 has yet to be determined.
methodsWe investigated the role of RPS23RG1 in maintaining synaptic structure and function in cell cultures and in Rps23rg1 knockout mice and determined whether targeting RPS23RG1-mediated pathways has therapeutic potential in APP/PS1 AD model mice.
resultsDeletion of the Rps23rg1 gene resulted in severe memory deficits and impairment of postsynaptic structure and function, with marked reductions in postsynaptic densities-93 and -95 (PSD-93 and PSD-95) levels. RPS23RG1 interacted with PSD-93/PSD-95 through its intracellular domain, consequently sequestering PSD-93/PSD-95 from murine double minute 2-mediated ubiquitination and degradation, thereby maintaining synaptic function. Restoration of PSD-93/PS-D95 levels reversed synaptic and memory deficits in Rps23rg1 knockout mice. We further observed attenuated RPS23RG1 expression in human AD, which positively correlated with PSD-93/PSD-95 levels. Importantly, an RPS23RG1-derived peptide comprising a unique PSD-93/PSD-95 interaction motif rescued synaptic and cognitive defects in Rps23rg1 knockout and AD mouse models.
conclusionsOur results reveal a role for RPS23RG1 in maintaining synaptic integrity and function and provide a new mechanism for synaptic dysfunction in AD pathogenesis. This demonstrates that RPS23RG1-mediated pathways show good therapeutic potential in AD intervention.
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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.