Title:Lithium Chloride Improves Electrophysiological and Memory Deficits in Rats with Streptozotocin-Induced Alzheimer's Disease
Volume: 22
Issue: 7
Author(s): Zheng Xing*, Xiaolian Jiang, Wenhao Yang, Yuhui Wang, Xiaoxiao Zhang and Chen Zhao*
Affiliation:
- School of Pharmacy, Changzhou University, Changzhou, Jiangsu, 213164, P.R. China
- Department of Pharmacy, The Second People's Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical University, Changzhou, Jiangsu, 213004, P.R. China
- Department of Pharmacy, The Second People's Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical University, Changzhou, Jiangsu, 213004, P.R. China
Keywords:
Alzheimer's disease, lithium chloride, electrophysiology, neuroprotective effect, GSK-3β, cognitive decline.
Abstract:
Introduction: Alzheimer's disease (AD) is a neurodegenerative disorder of the central
nervous system characterized by complex pathological manifestations and an unclear pathogenesis.
Lithium chloride (LiCl) exhibits certain neuroprotective effects. However, its performance
and mechanisms in different types of AD models remain unclear.
Methods: The streptozotocin (STZ)-induced AD rat model was used to evaluate the ameliorating
effects of LiCl. LiCl was administered orally for one month, and then evaluations were conducted
in terms of nerve electrophysiology, behavioral science, and molecular biology.
Results: In this study, STZ was found to significantly affect the electrophysiological functions
and behavioral performances of rats. However, LiCl was able to mitigate these effects. Specifically,
it led to the restoration of electrophysiological functions, with long-term potentiation (LTP) being
successfully induced. LiCl also demonstrated favorable therapeutic effects in rats, as confirmed
by the nest-building tests, Y-maze, and Morris water maze. Further research revealed that
LiCl promoted the phosphorylation of GSK-3β in the hippocampal region of rats.
Discussion: These findings indicated that LiCl demonstrated beneficial effects on AD-like pathological
changes in STZ-induced AD rats, possibly by activating GSK-3β phosphorylation in the
hippocampus, improving electrophysiological functions, and further restoring behavioral characteristics.
Conclusion: In conclusion, LiCl demonstrated therapeutic potential for AD by improving neurophysiological
and behavioral deficits via hippocampal GSK-3β phosphorylation.