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Updated: Jul 22, 2026
Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
Published on: February 13, 2014
High uric acid induced hippocampal mitochondrial dysfunction and cognitive impairment involving intramitochondrial
Chun Shi1,2, Han Guo1, Xintong Liu2
1Department of Anatomy, Dali University, Dali.
Objectives:
Epidemiological research has indicated that hyperuricemia may impair cognitive ability; however, the underlying mechanisms remain unclear. The present study thus investigated the possible mechanism underlying hyperuricemia-related cognitive impairment.
Methods:
Using hyperuricemic rats and high uric acid (UA) intracerebroventricularly treated mice, the current study elucidated whether and how high UA impaired cognitive ability and hippocampal mitochondrial bioenergetic function.
Results:
Hyperuricemia induced UA uptake by hippocampal mitochondria, which impaired cognitive ability and disrupted the bioenergetic function of hippocampal mitochondria, indicated by reduced ATP production and decreased cytochrome c oxidase (COX) activity. Mechanistically, excess UA might trigger intramitochondrial NF-κB inhibitor α (IκBα)/nuclear factor-κB (NF-κB) pathway to downregulate the subunit III of COX (COXIII).
Conclusion:
The results provided new insights into the mechanism underlying hyperuricemia-related cognitive decline.
