ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2025
Nicotinamide Prevents the Plasticity Impairments and the Cognitive Dysfunction Caused by Bone Fracture in Older Mice.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 2 of them syntheses that pooled it.
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Who cites it
4 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Inflammation and delirium in critically Ill patients: a review.Frontiers in aging neuroscience · 2026Pooled it
- The effect of ciprofol on the incidence of postoperative delirium in adult surgical patients: a meta-analysis and meta-regression.Frontiers in neurologyPooled it
- Restoring NADFrontiers in nutrition · 2026Review
- Frailty and prolonged preoperative waiting time as independent predictors of postoperative delirium in older hip fracture patients.Scientific reports · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Postoperative delirium (POD), an acute cognitive dysfunction linked to morbidity and mortality, is characterized by memory impairments and disturbances in consciousness, particularly in patients aged 65 and older. Neuroinflammation and NAD+ imbalance are key mechanisms behind POD, leading to synaptic and cognitive deterioration. However, how surgery contributes to POD and neuroinflammation remains unclear, and effective treatments are lacking. Here we used a rodent model of bone fracture to examine the impact of surgery on synaptic plasticity, inflammation, and cognition. Additionally, we explored whether treatment with nicotinamide (NAM), a NAD+ precursor, reduced the neuroinflammation and metabolic imbalance caused by surgery. Female C57BL/6J mice aged 20-22 months underwent tibial fracture surgery and received pre- and post-surgery NAM treatment. Neuroinflammation, synaptic plasticity, and cognition were assessed 72 hours post-surgery via long-term potentiation (LTP) assays, dendritic spine counting, and behavioral tests (open field maze and Y-maze). Tibial fracture surgery decreased LTP, dendritic spine density, and hippocampal-dependent memory function, and increased hippocampal inflammatory markers (IL-1β mRNA, CD38, and SIRT1 protein content); NAM pretreatment prevented these changes. Given surgery's adverse effects on LTP and dendritic spine density, we assessed cellular oxidative state and brain-derived neurotrophic factor (BDNF) protein levels. We found that surgery increased the oxidation of ryanodine receptor calcium channels (cellular redox sensors), and decreased BDNF protein levels; NAM supplementation mitigated both effects and prevented the cognitive decline and synaptic plasticity deficits while reducing inflammation post-surgery by lowering IL-1β and CD38 protein levels. We propose that the CD38 signaling pathway mediates these NAM protective effects.
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Registered trials
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