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Related Experiment Video

Updated: Jan 27, 2026

Brain Imaging Investigation of the Impairing Effect of Emotion on Cognition

Brain Imaging Investigation of the Impairing Effect of Emotion on Cognition

Published on: February 1, 2012

FGF-23 Deficiency Impairs Hippocampal-Dependent Cognitive Function.

Ann M Laszczyk¹, Dailey Nettles¹, Tate A Pollock¹

¹Department of Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294.

|March 27, 2019

Summary

This summary is machine-generated.

Fibroblast growth factor 23 (FGF-23) deficiency impairs hippocampal-dependent cognition in mice. Unlike Klotho deficiency, FGF-23 deficiency does not cause major brain structural or neurogenesis defects.

Keywords:

post-natal neurogenesis seizure synaptic transmission

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Area of Science:

Neuroscience
Endocrinology
Aging Research

Background:

Fibroblast growth factor receptor (FGFR) and α-Klotho mediate FGF-23 signaling for phosphate and vitamin D homeostasis.
Both FGF-23 and Klotho deficiency in mice lead to premature aging-like phenotypes, suggesting co-dependent functions.
Klotho deficiency impacts central nervous system (CNS) functions, including cognition, but FGF-23's effects on the brain remain unclear.

Purpose of the Study:

To investigate the effects of FGF-23 deficiency on hippocampal function and cognition.
To compare the brain phenotype of FGF-23-deficient mice with that of Klotho-deficient mice.

Main Methods:

Assessment of cognitive function in FGF-23-deficient mice.
Analysis of brain structure, synaptic plasticity, and neurogenesis in FGF-23-deficient brains.
Comparative analysis with existing data on Klotho-deficient mice.

Main Results:

FGF-23-deficient mice exhibit dose-dependent, hippocampal-dependent cognitive impairment.
FGF-23 deficiency did not result in gross structural or developmental brain defects.
No significant changes in hippocampal synaptic plasticity were observed, with only minor impairment in postnatal neurogenesis.

Conclusions:

FGF-23 plays a crucial role in maintaining hippocampal-dependent cognitive function.
The brain phenotype associated with FGF-23 deficiency is distinct from that observed in Klotho-deficient mice, despite similarities in systemic aging phenotypes.