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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4962599 | PMC |
| http://dx.doi.org/10.4103/1673-5374.184500 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Association between herpes simplex virus infection and Alzheimer's disease biomarkers: analysis within the MAPT trial.
Sci Rep
January 2025
INSERM, Bergonié Institute, BPH, U1219, CIC-P 1401, University of Bordeaux, Bordeaux, France.
In vitro and animal studies have suggested that inoculation with herpes simplex virus 1 (HSV-1) can lead to amyloid deposits, hyperphosphorylation of tau, and/or neuronal loss. Here, we studied the association between HSV-1 and Alzheimer's disease biomarkers in humans. Our sample included 182 participants at risk of cognitive decline from the Multidomain Alzheimer Preventive Trial who had HSV-1 plasma serology and an amyloid PET scan.
View Article and Find Full Text PDFTreadmill Exercise Mitigates Alzheimer's Pathology by Modulating Glial Polarization and Reducing Oligodendrocyte Precursor Cell Perivascular Clustering.
Med Sci Sports Exerc
January 2025
School of Physical Education and Sports Science, South China Normal University, Guangzhou, CHINA.
Purpose: This study aimed to investigate the pathological responses of glial cells at different distances from amyloid plaques and the characteristics of oligodendrocyte precursor cells (OPCs) in perivascular clustering. Additionally, it sought to explore the impact of exercise training on AD pathology, specifically focusing on the modulation of glial responses and the effects of OPC perivascular clustering.
Methods: Three-month-old C57BL/6 and APP/PS1 mice were divided into four groups: wild-type sedentary, wild-type exercise, sedentary AD, and exercise AD groups.
Multi-Targeting Phytochemicals for Alzheimer's Disease.
Phytother Res
January 2025
Department of Pharmaceutical Sciences, Hemwati Nandan Bahuguna Garhwal University (A Central University), Srinagar, Uttarakhand, India.
Alzheimer's disease (AD) is a type of neurodegenerative illness in which β-amyloid (Aβ) and tau protein accumulate in neurons in the form of tangles. The pathophysiological pathway of AD consists of Aβ-amyloid peptides, tau proteins, and oxidative stress in neurons and increased neuro-inflammatory response. Food and Drug Administration in the United States has authorized various drugs for the effective treatment of AD, which include galantamine, rivastigmine, donepezil, memantine, sodium oligomannate, lecanemab, and aducanumab.
View Article and Find Full Text PDFDiscovering potential ERK1 inhibitors from natural products for therapeutic targeting of Alzheimer's disease.
J Alzheimers Dis
January 2025
Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi, India.
Background: Extracellular signal-regulated kinase 1 (ERK1) belongs to mitogen-activated protein kinases, which are essential for memory formation, cognitive function, and synaptic plasticity. During Alzheimer's disease (AD), ERK1 phosphorylates tau at 15 phosphorylation sites, leading to the formation of neurofibrillary tangles. The overactivation of ERK1 in microglia promotes the release of pro-inflammatory cytokines, which results in neuroinflammation.
View Article and Find Full Text PDFEnvironmental Mycotoxins: A Potential Etiological Factor for Neurodegenerative Diseases?
Toxicology
January 2025
College of Life Science, Yangtze University, Jingzhou 434025, China. Electronic address:
Mycotoxins are potential environmental risk factors for neurodegenerative diseases. These toxins penetrate the central nervous system via a compromised blood-brain barrier, which may cause oxidative stress and neuroinflammation, these can also contribute to amyloid-beta (Aβ) plaque accumulation, Tau protein hyperphosphorylation, and neurofibrillary tangle formation. Mycotoxins also activate microglia, cause neuronal apoptosis, and disrupt central nervous system function.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!