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Fingolimod affects gene expression profile associated with LPS-induced memory impairment
Rana Omidbakhsh1, Banafshe Rajabli, Sanaz Nasoohi
1Department of Pharmacology, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Experimental Brain Research
|August 8, 2014
Summary
Fingolimod (FTY720) effectively treats lipopolysaccharide-induced memory impairment in rats, whether given before or after the endotoxin. This suggests FTY720 benefits neuroinflammation regardless of preventive or therapeutic application.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Lipopolysaccharide (LPS) induces sickness behavior and cognitive deficits.
- Neuroinflammation is a key factor in disease progression, influenced by sphingosine-1-phosphate.
- Fingolimod (FTY720), a sphingosine analog, impacts gene expression in Alzheimer's disease models.
Purpose of the Study:
- To evaluate fingolimod's efficacy in mitigating memory impairment caused by neuroinflammation.
- To determine if FTY720 is more effective as a preventive or therapeutic agent against LPS-induced effects.
Main Methods:
- Rats received FTY720 before or after intracerebral LPS injection.
- Memory performance was assessed using a passive avoidance test.
- Brain tissue underwent histological and multiplex mRNA assays (QuantiGene Plex).
Main Results:
- Both FTY720 pre-treatment and post-treatment significantly ameliorated LPS-induced memory impairment.
- FTY720 administration altered transcriptional levels of mitogen-activated protein kinases and inflammatory genes.
- The drug's efficacy was comparable in both preventive and therapeutic settings.
Conclusions:
- Fingolimod (FTY720) effectively reverses LPS-induced memory deficits in rats.
- FTY720's benefits against neuroinflammation are evident whether used preventively or therapeutically.
- These findings support FTY720's potential in managing neuroinflammatory conditions impacting cognition.
