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sh-sy5y-cells
8 studies tagged sh-sy5y-cells, dated 2010-06-04 to 2021-02-22. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- The Impact of Differentiation on Cytotoxicity and Insulin Sensitivity in Streptozotocin Treated SH-SY5Y Cells 2021-02-22
- Liraglutide Attenuates Aβ42 Generation in APPswe/SH-SY5Y Cells Through the Regulation of Autophagy 2020-07-27
- The protective effects of liraglutide on AD-like neurodegeneration induced by oxidative stress in human neuroblastoma SH-SY5Y cells 2019-06-04
Studies
8 studies carry this tag.
Date range
2010 to 2021
Top journals
- Applied biochemistry and biotechnology 1
- Chemico-biological interactions 1
- International journal of molecular sciences 1
- Journal of neuroscience methods 1
- Neurochemical research 1
8 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Recently neuronal insulin resistance was suggested playing a role in Alzheimer's disease.
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Here, we report a novel mechanism underlying liraglutide-attenuated Aβ42 generation through the activation of autophagy in AD cellular model.
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Glucagon-like peptide 1 (GLP-1) has neuroprotective properties in Alzheimer's disease (AD).
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Alzheimer's disease (AD) is a major neurodegenerative disease, associated with the hallmark proteinacious constituent called amyloid beta (Aβ) of senile plaques.
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Our data provide a novel characterization of an OA-based cell culture model in which OA induces the appearance of HMW-TIPs.
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Neuroblastoma cell lines such as SH-SY5Y are the most frequently utilized models in neurodegenerative research, and their use has advanced the understanding of the pathology of neurodegeneration over the past few decades.
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These findings suggest that liraglutide prevented Aβ (25-35)-induced neurotoxicity by inhibiting neuronal apoptosis and liraglutide may have a neuroprotective effect through activation of the PI3K/Akt signaling pathway.
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As aged population dramatically increases in these decades, efforts should be made on the intervention for curing age-associated neurologic degenerative diseases such as Alzheimer's disease (AD).