FGF-23 deficiency impairs hippocampal-Dependent cognitive function

Ann M. Laszczyk, Dailey Nettles, Tate A. Pollock, Stephanie Fox, Melissa L. Garcia, Jing Wang, L. Darryl Quarles, Gwendalyn D. King

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


Fibroblast growth factor receptor (FGFR) and α-Klotho transduce FGF-23 signaling in renal tubules to maintain systemic phosphate/vitamin D homeostasis. Mice deficient for either the ligand, FGF-23, or the co-receptor, Klotho, are phenocopies with both showing rapid and premature development of multiple aging-like abnormalities. Such similarity in phenotype, suggests that FGF-23 and Klotho have co-dependent systemic functions. Recent reports revealed inverse central nervous system (CNS) effects of Klotho deficiency or Klotho overexpression on hippocampal synaptic, neurogenic, and cognitive functions. However, it is unknown whether FGF-23 deficiency effects function of the hippocampus. We report that, similar to Klotho-deficient mice, FGF-23-deficient mice develop dose-dependent, hippocampal-dependent cognitive impairment. However, FGF-23-deficient brains had no gross structural or developmental defects, no change in hippocampal synaptic plasticity, and only minor impairment to postnatal hippocampal neurogenesis. Together, these data provide evidence that FGF-23 deficiency impairs hippocampal-dependent cognition but otherwise results in a brain phenotype that is distinct from the KL-deficient mouse.

Original languageEnglish (US)
Article numbere0469-18.2019
Issue number2
StatePublished - Mar 1 2019
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)


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