ArticleMolecular neurobiology2014
Amelioration of diabetes-induced cognitive deficits by GSK-3β inhibition is attributed to modulation of neurotransmitters and neuroinflammation.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 77 citations in OpenAlex.
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- Tirzepatide mitigates cognitive decline in zebrafish model of type 2 diabetes mellitus induced by high-fat diet.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Aerobic exercise and metformin attenuate the cognitive impairment in an experimental model of type 2 diabetes mellitus: focus on neuroinflammation and adult hippocampal neurogenesis.Metabolic brain disease · 2025Article
- Memory improving effect of silkworm larva on insulin resistance related cognitive impairment model.PloS one · 2025Article
- GSK3-Driven Modulation of Inflammation and Tissue Integrity in the Animal Model.International journal of molecular sciences · 2024Review
- Article
- YQBS Improves Cognitive Dysfunction in Diabetic Rats: Possible Association with Tyrosine and Tryptophan Metabolism.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- CaMKIV/CREB/BDNF signaling pathway expression in prefrontal cortex, amygdala, hippocampus and hypothalamus in streptozotocin-induced diabetic mice with anxious-like behavior.Experimental brain research · 2022Article
- Crosstalk between neurological, cardiovascular, and lifestyle disorders: insulin and lipoproteins in the lead role.Pharmacological reports : PR · 2022Review
- Neuroprotective Effect of 2-Aminoethoxydiphenyl Borate (2-APB) in Amyloid β-Induced Memory Dysfunction: A Mechanistic Study.Cellular and molecular neurobiology · 2022Article
- Advances in PPARs Molecular Dynamics and Glitazones as a Repurposing Therapeutic Strategy through Mitochondrial Redox Dynamics against Neurodegeneration.Current neuropharmacology · 2022Review
- Potential Glioprotective Strategies Against Diabetes-Induced Brain Toxicity.Neurotoxicity research · 2021Review
- The mTOR/NF-κB Pathway Mediates Neuroinflammation and Synaptic Plasticity in Diabetic Encephalopathy.Molecular neurobiology · 2021Article
- The Role of Molecular and Inflammatory Indicators in the Assessment of Cognitive Dysfunction in a Mouse Model of Diabetes.International journal of molecular sciences · 2021Article
- Review
- Aerobic Exercise Improves Synaptic-Related Proteins of Diabetic Rats by Inhibiting FOXO1/NF-κB/NLRP3 Inflammatory Signaling Pathway and Ameliorating PI3K/Akt Insulin Signaling Pathway.Journal of molecular neuroscience : MN · 2019Article
- Quetiapine Attenuates the Neuroinflammation and Executive Function Deficit in Streptozotocin-Induced Diabetic Mice.Mediators of inflammation · 2019Article
- The Relevance of Insulin Action in the Dopaminergic System.Frontiers in neuroscience · 2019Review
- Mechanisms underlying the role of DISC1 in synaptic plasticity.The Journal of physiology · 2018Review
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Chronic type 2 diabetes (T2D) causes cognitive deficits which are debilitating to the young as well as the older population. Glycogen synthase kinase-3β (GSK-3β) signaling has been reported to be impaired in insulin-resistant and T2D animal models. In this study, we have investigated the involvement of GSK-3β in cognitive deficits associated with T2D using SB216763, a GSK-3 β inhibitor. In high-fat diet-streptozotocin (HFD-STZ) model of T2D in rats, cognitive deficits appeared on the 15th week after induction of diabetes. Treatment with GSK-3β inhibitor SB216763 (i.p. daily for 3 weeks) reversed impaired cognitive performance in the Morris water maze, Y-maze, and passive avoidance tests. Administration of SB216763 also significantly improved acetylcholine esterase activity, GABA, and glutamate levels in the hippocampus and cortex of diabetic rats. Importantly, GSK-3β inhibition showed an increase in pGSK-3β and pCREB expression and reduction in pNF-κB-p65 expression in both hippocampus and cortex. Neuroinflammation was reduced by SB216763 in diabetic rats as evident from reduction in IL-6, TNF-α, COX-2, and inducible nitric oxide synthase levels. This study suggests that cognitive deficits associated with diabetes involved intricate compartmental interaction between transcription factors and neurotransmitter homeostasis/energy metabolism, and GSK-β might play a central role in diabetes-induced cognitive impairment.
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