Lithium Chloride Improves Electrophysiological and Memory Deficits in Rats with Streptozotocin-Induced Alzheimer's Disease.

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.