ArticlePsychopharmacology2026
Integrated stress response inhibition rescues inflammation-associated accelerated forgetting of recognition memory in mice.
Article in Psychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Distinct cell type-specific mechanisms underlie cognitive dysfunction during persistent integrated stress response activation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
rationaleAccelerated forgetting contributes substantially to memory deterioration in various neurological disorders in which inflammation is a prominent pathological hallmark. Inflammation typically impairs memory formation. Given that the neural mechanisms underpinning forgetting may be associated with that supporting memory formation, inflammation could be a key driver of accelerated forgetting. However, this assumption and its mechanistic basis have not been systematically examined.
objectivesTo determine whether lipopolysaccharide (LPS), a robust inducer of systemic inflammation, accelerates the forgetting of recognition memory, and whether the integrated stress response (ISR) plays a mechanistic role in this process.
methodsMice were trained based on two recognition memory paradigms and subsequently received vehicle, LPS, or LPS combined with the ISR inhibitor ISRIB during the memory retention interval. Sickness behavior was assessed by monitoring body weight and food intake. Memory performance was quantified using the exploration index reflecting novelty preference. Microglial and ISR activation in the hippocampus were evaluated via examining the expression of Iba1, phosphorylated eukaryotic translation initiation factor 2α (p-eIF2α), and activating transcription factor 4 (ATF4), respectively.
resultsLPS elicited marked sickness behaviors, accelerated the decay of previously acquired recognition memory, and triggered robust microglial and ISR activation in the hippocampus. ISRIB administration effectively reversed LPS-provoked microglial and ISR activation, and accelerated forgetting, while leaving sickness behaviors and memory retrieval unaffected.
conclusionsLPS-elicited inflammation accelerates the forgetting of recognition memory, and ISR activation is involved in this effect, suggesting that ISR inhibition may provide a potential therapeutic target for inflammation-associated accelerated forgetting.
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Registered trials
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