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Updated: Mar 16, 2026
Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
Published on: November 9, 2018
Indirubin-3'-monoxime suppresses amyloid-beta-induced apoptosis by inhibiting tau hyperphosphorylation
Shu-Gang Zhang1, Xiao-Shan Wang1, Ying-Dong Zhang2
1Department of Neurology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Abstract:
Indirubin-3'-monoxime is an effective inhibitor of cyclin-dependent protein kinases, and may play an obligate role in neuronal apoptosis in Alzheimer's disease. Here, we found that indirubin-3'-monoxime improved the morphology and increased the survival rate of SH-SY5Y cells exposed to amyloid-beta 25-35 (Aβ25-35), and also suppressed apoptosis by reducing tau phosphorylation at Ser199 and Thr205. Furthermore, indirubin-3'-monoxime inhibited phosphorylation of glycogen synthase kinase-3β (GSK-3β). Our results suggest that indirubin-3'-monoxime reduced Aβ25-35-induced apoptosis by suppressing tau hyperphosphorylation via a GSK-3β-mediated mechanism. Indirubin-3'-monoxime is a promising drug candidate for Alzheimer's disease.
Insights
Indirubin-3'-monoxime protects neuronal cells from amyloid-beta toxicity in Alzheimer's disease models. This compound reduces apoptosis and tau hyperphosphorylation, suggesting therapeutic potential.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Alzheimer's disease is characterized by neuronal apoptosis and tau hyperphosphorylation.
- Amyloid-beta (Aβ25-35) exposure induces apoptosis in neuronal cells.
- Indirubin-3'-monoxime inhibits cyclin-dependent protein kinases.
Purpose of the Study:
- To investigate the neuroprotective effects of indirubin-3'-monoxime against Aβ25-35-induced apoptosis.
- To elucidate the mechanism underlying the protective effects of indirubin-3'-monoxime.
Main Methods:
- SH-SY5Y cells were exposed to Aβ25-35.
- The effects of indirubin-3'-monoxime on cell morphology, survival rate, and apoptosis were assessed.
- Tau phosphorylation at Ser199 and Thr205, and glycogen synthase kinase-3β (GSK-3β) phosphorylation were measured.
Main Results:
- Indirubin-3'-monoxime improved cell morphology and increased survival rate in Aβ25-35-treated SH-SY5Y cells.
- Indirubin-3'-monoxime suppressed apoptosis by reducing tau phosphorylation at Ser199 and Thr205.
- Indirubin-3'-monoxime inhibited GSK-3β phosphorylation.
Conclusions:
- Indirubin-3'-monoxime mitigates Aβ25-35-induced neuronal apoptosis.
- The protective mechanism involves the suppression of tau hyperphosphorylation via GSK-3β inhibition.
- Indirubin-3'-monoxime shows promise as a therapeutic agent for Alzheimer's disease.
