Background: In previous studies, we found that quetiapine activates the AKT signaling which further inhibits the action of GSK3β. Quetiapine has been reported to possess neuroprotective potential in schizophrenia and other neurodegenerative models.
Method: On day 1 and 3, rats received bilateral intracerebroventricular (i.c.v.) administration of STZ (3 mg/kg). From day 8 to day 21 of treatment of quetiapine, a GSK3-β inhibitor and neuroprotective medication, was given at dose levels of 2.5, 5, and 10 mg/kg/i.p. Morris water maze and Object recognition test was performed for the evaluation of cognitive impairment, whereas biochemical, histopathological, neuroinflammatory were evaluated by hippocampal and cortical brain region on 22 day.
Result: ICV-STZ results in cognitive impairment, spatial and non-special learning deficit in OFT, MWM and ORT tests respectively, including elevation in the levels of nitrite and MDA and decreased antioxidant enzymes GSH, SOD and Catalase levels, also produced degenerative changes in dentate gyrus, CA1, CA2 and CA3 region of hippocampus as well as cortex in rat brains. Whereas, Quetiapine treatment significantly attenuated STZ-induced cognitive deficit, oxidative stress and improved density of surviving neurons in hippocampal/cortical region of rat brains.
Conclusion: The conclusive outcomes of the present study, clearly indicate neuroprotective potential of quetiapine in neurodegenerative pathogenesis associated with cognitive dysfunction.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/alz.088739 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Electroacupuncture attenuates ferroptosis by promoting Nrf2 nuclear translocation and activating Nrf2/SLC7A11/GPX4 pathway in ischemic stroke.
Chin Med
January 2025
Yunnan Key Laboratory of Integrated Traditional Chinese and Western Medicine for Chronic Disease in Prevention and Treatment, Key Laboratory of Acupuncture and Massage for Treatment of Encephalopathy, College of Acupuncture, Tuina and Rehabilitation, Yunnan University of Traditional Chinese Medicine, Kunming, China.
Objective: Electroacupuncture has been shown to play a neuroprotective role following ischemic stroke, but the underlying mechanism remains poorly understood. Ferroptosis has been shown to play a key role in the injury process. In the present study, we wanted to explore whether electroacupuncture could inhibit ferroptosis by promoting nuclear factor erythroid-2-related factor 2 (Nrf2) nuclear translocation.
View Article and Find Full Text PDFDihuang Yinzi Improves Scopolamine-Induced Learning and Memory Impairment by Regulating Plasma Exosome-Derived BDNF.
J Ethnopharmacol
January 2025
School of Basic Medical Sciences, Shanxi University of Chinese Medicine, Jinzhong, Shanxi, 030619; Shanxi Provincial Key Laboratory of TCM Encephalopathy; National International Joint Research Center for Molecular Traditional Chinese Medicine. Electronic address:
Ethnopharmacological Relevance: Dihuang Drink (DHD), formulated by Liu Hejian during the Yuan Dynasty, is listed as one of the first ancient classical prescriptions by the National Medical Products Administration of China. It is commonly used for the prevention and treatment of Alzheimer's disease (AD). This study further investigates the therapeutic effects and potential mechanisms of DHD in AD.
View Article and Find Full Text PDFIndole and Coumarin Derivatives Targeting EEF2K in Aβ Folding Reporter Cells.
J Neurochem
January 2025
Department of Neurology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Misfolding and accumulation of amyloid-β (Aβ) in the brains of patients with Alzheimer's disease (AD) lead to neuronal loss through various mechanisms, including the downregulation of eukaryotic elongation factor 2 (EEF2) protein synthesis signaling. This study investigated the neuroprotective effects of indole and coumarin derivatives on Aβ folding and EEF2 signaling using SH-SY5Y cells expressing Aβ-green fluorescent protein (GFP) folding reporter. Among the tested compounds, two indole (NC009-1, -6) and two coumarin (LM-021, -036) derivatives effectively reduced Aβ misfolding and associated reactive oxygen species (ROS) production.
View Article and Find Full Text PDFMagnolia kobus DC. suppresses neointimal hyperplasia by regulating ferroptosis and VSMC phenotypic switching in a carotid artery ligation mouse model.
Chin Med
January 2025
Aging and Metabolism Research Group, Korea Food Research Institute, Wanju‑gun, 55365, Republic of Korea.
Background: Magnolia kobus DC (MO), as a plant medicine, has been reported to have various physiological activities, including neuroprotective, anti-inflammatory, and anti-diabetic effects. However, vascular protective effects of MO remain incompletely understood. In this study, we evaluated the vascular protective effect of MO against ferroptosis in a carotid artery ligation (CAL)-induced neointimal hyperplasia mouse model and in aortic thoracic smooth muscle A7r5 cells.
View Article and Find Full Text PDFTargeting uric acid: a promising intervention against oxidative stress and neuroinflammation in neurodegenerative diseases.
Cell Commun Signal
January 2025
Department of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, 758 Hefei Road, Qingdao, China.
Oxidative stress and neuroinflammation are recognized as key factors in the development of neurodegenerative diseases, yet effective interventions and biomarkers to address oxidative stress and neuroinflammation in these conditions are limited. Uric acid (UA), traditionally associated with gout, is now gaining prominence as a potential target in neurodegenerative diseases. Soluble UA stands out as one of the most vital antioxidant compounds produced by the human body, accounting for up to 55% of the extracellular capacity to neutralize free radicals.
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!