ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Phosphorylated Glycogen Synthase Kinase-3β (GSK-3β) Improves Cognition in Rats with Diabetes-Associated Cognitive Decline.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- AdipoRon Ameliorates Synaptic Dysfunction and Inhibits tau Hyperphosphorylation through the AdipoR/AMPK/mTOR Pathway in T2DM Mice.Neurochemical research · 2024Article
- Retracted: Phosphorylated Glycogen Synthase Kinase-3β (GSK-3β) Improves Cognition in Rats with Diabetes-Associated Cognitive Decline.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
Corrections and comments
- Retraction · 2019-08-21Duplication of/in Image ·
- Retracted
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The serine/threonine kinase glycogen synthase kinase-3ß (GSK-3ß) is involved in a broad range of cellular processes, including cell proliferation, apoptosis, and inflammation. GSK-3ß has been considered to play an important role in the pathogenesis of T2DM and AD, which is activated in both the periphery and central nervous system. However, the upstream and downstream factors and the underlying regulatory mechanisms of GSK-3ß in T2DM and AD are unclear. MATERIAL AND METHODS Here, we investigated the production of cytochrome C, Caspase-3, and Caspase-9 in in the hippocampus of DM rats and clarify the role of GSK-3ß in these processes. Streptozotocin (STZ)-induced DM rats presented increased GSK-3ß activity. RESULTS We found that cytochrome C, Caspase-3, and Caspase-9 were overproduced in the hippocampus. Furthermore, the cytochrome C, Caspase-3, and Caspase-9 levels were restored after GSK-3ß inhibitors Licl treatment. CONCLUSIONS Our results show that GSK-3ß regulates the production of cytochrome C, Caspase-3, and Caspase-9 in STZ-induced rat brain and may therefore contribute to DM-caused cognitive dysfunction via inhibition of neural cell apoptosis.
Identifiers
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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.