ArticleMolecular neurobiology2015
Activation of Glycogen Synthase Kinase-3 Mediates the Olfactory Deficit-Induced Hippocampal Impairments.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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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
16 citing papers in PubMed, 30 citations in OpenAlex.
- Moxa-combustion byproducts improve cognitive function via olfactory-mediated modulation of the GSK-3β/CREB pathway.Frontiers in neuroscience · 2026Article
- Ceramides may Play a Central Role in the Pathogenesis of Alzheimer's Disease: a Review of Evidence and Horizons for Discovery.Molecular neurobiology · 2025Review
- A Mouse Model of Sporadic Alzheimer's Disease with Elements of Major Depression.Molecular neurobiology · 2025Article
- Senktide blocks aberrant RTN3 interactome to retard memory decline and tau pathology in social isolated Alzheimer's disease mice.Protein & cell · 2024Article
- Cdc42 Facilitates Axonogenesis by Enhancing Microtubule Stabilization in Primary Hippocampal Neurons.Cellular and molecular neurobiology · 2021Article
- Preventive electroacupuncture reduces cognitive deficits in a rat model of D-galactose-induced aging.Neural regeneration research · 2021Article
- Loss of ferroportin induces memory impairment by promoting ferroptosis in Alzheimer's disease.Cell death and differentiation · 2021Article
- Preventive Electroacupuncture Ameliorates D-Galactose-Induced Alzheimer's Disease-Like Pathology and Memory Deficits Probably via Inhibition of GSK3Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Ginsenoside Rb1 ameliorates cisplatin-induced learning and memory impairments.Journal of ginseng research · 2019Article
- Hippocampus Metabolic Disturbance and Autophagy Deficiency in Olfactory Bulbectomized Rats and the Modulatory Effect of Fluoxetine.International journal of molecular sciences · 2019Article
- Activation of MT2 receptor ameliorates dendritic abnormalities in Alzheimer's disease via C/EBPα/miR-125b pathway.Aging cell · 2019Article
- Suppression of microRNA-9-5p rescues learning and memory in chronic cerebral hypoperfusion rats model.Oncotarget · 2017Article
- Lentiviral Modulation of Wnt/β-Catenin Signaling Affects In Vivo LTP.Cellular and molecular neurobiology · 2017Article
- Role of microtubule-associated protein tau phosphorylation in Alzheimer's disease.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017Review
- Cnga2 Knockout Mice Display Alzheimer's-Like Behavior Abnormities and Pathological Changes.Molecular neurobiology · 2016Article
- Olfactory Deprivation Hastens Alzheimer-Like Pathologies in a Human Tau-Overexpressed Mouse Model via Activation of cdk5.Molecular neurobiology · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The populations with olfactory dysfunction show an increased chance for hippocampus-dependent episodic memory deficit. Although it is known that the olfactory information projects to the hippocampus through entorhinal cortex layer II, the molecular mechanisms linking olfactory deficit to the hippocampus is not understood. Using bilateral olfactory bulbectomy (OBX) as a model, we found that OBX induced memory deficits with activation of several memory-related protein kinases in the hippocampal extracts, including glycogen synthase kinase-3β (GSK-3β), protein kinase A (PKA), extracellular-signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-kinase (PI3K), and protein kinase B (PKB). The OBX rats also show suppression of long-term potentiation (LTP); reduction of synapsin I, synaptophysin, NR2A/B, and PSD95; thinner presynaptic active zone and postsynaptic density with enlarged synaptic space; decreased spine numbers and mushroom-type spines; and tau hyperphosphorylation. After injection of SB216763 for several weeks by vena caudalis, selective inhibition of GSK-3β ameliorated the OBX-induced memory deficits with recovery of the synaptic components and tau phosphorylation. Furthermore, genetic ablation of GSK-3β by lentivirus-packed shRNA effectively rescued the memory deficits, synaptic disorder, and tauopathy. Our data indicate that GSK-3 activation mediates the olfactory deficits to the hippocampus, and targeting GSK-3 blocks the pathological connection.
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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.