ArticleNeural regeneration research2026
Mechanism of action of synaptic mitochondrial damage in delayed cognitive recovery.
Article in Neural regeneration research, 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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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.
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Who cites it
1 citing paper in PubMed.
- Increased reactive astrocytes in hippocampal CA1 region mediated by decreased CXCR7 is involved in postoperative cognitive dysfunction in aged mice.Cell biology and toxicology · 2025Article
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10 authors.
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No grant is acknowledged in the PubMed record.
Abstract
JOURNAL/nrgr/04.03/01300535-202606000-00060/figure1/v/2026-02-11T151048Z/r/image-tiff Delayed neurocognitive recovery following anesthesia and surgery is a common complication in older adult patients. Synapses are fundamental to cognitive function. The activity of synapses heavily depends on the energy supplied by synaptic mitochondria, which are significantly influenced by oxidative stress. Sirtuin 3 is a histone deacetylase located in the mitochondrial matrix that plays a pivotal role in regulating mitochondrial function. However, it remains unclear whether and how sirtuin 3 is involved in the development of delayed cognitive recovery. Therefore, in this study, we investigated the potential role of sirtuin 3 in synapses during delayed neurocognitive recovery. Our results showed that anesthesia and surgery induced cognitive impairment in mice and reduced sirtuin 3 protein expression. Overexpression of sirtuin 3 inhibited opening of the mitochondrial permeability transition pore by reducing acetylation of K166 on cyclophilin D and also rescued cognitive impairment. Aged mice carrying the cyclophilin D-K166R mutation exhibited significantly reduced cognitive impairment. Similarly, administering the mitochondrial permeability transition pore blocker, cyclosporine A, effectively alleviated the decline in synaptic mitochondrial function and cognitive impairment caused by anesthesia and surgery in aged mice. These results indicate that the sirtuin 3/cyclophilin D-K166/mPTP signaling pathway in hippocampal synaptic mitochondria is involved in delayed neurocognitive recovery of aged mice, suggesting this pathway could serve as a potential target for treatment.
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