ArticleCurrent Alzheimer research2025
Lithium Chloride Improves Electrophysiological and Memory Deficits in Rats with Streptozotocin-Induced Alzheimer's Disease.
Article in Current Alzheimer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Article
- Intracerebroventricular streptozotocin-induced animal model of Alzheimer's disease: revealing dose optimization, administration regimen, and molecular pathways.Laboratory animal research · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
introductionAlzheimer'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.
methodsThe 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.
resultsIn 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.
conclusionIn conclusion, LiCl demonstrated therapeutic potential for AD by improving neurophysiological and behavioral deficits via hippocampal GSK-3β phosphorylation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.