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Neurobiol Aging. 2014 Jul;35(7):1769-77. doi: 10.1016/j.neurobiolaging.2013.12.023. Epub 2013 Dec 26.

Severe amygdala dysfunction in a MAPT transgenic mouse model of frontotemporal dementia.

Author information

1
Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL, USA.
2
Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL, USA; Neurobiology of Disease Program, Mayo Graduate School, Rochester, MN, USA.
3
Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL, USA; Neurobiology of Disease Program, Mayo Graduate School, Rochester, MN, USA. Electronic address: fryer.john@mayo.edu.

Abstract

Frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) is a neurodegenerative tauopathy caused by mutations in the tau gene (MAPT). Individuals with FTDP-17 have deficits in learning, memory, and language, in addition to personality and behavioral changes that are often characterized by a lack of social inhibition. Several transgenic mouse models expressing tau mutations have been tested extensively for memory or motor impairments, though reports of amygdala-dependent behaviors are lacking. To this end, we tested the rTg4510 mouse model on a behavioral battery that included amygdala-dependent tasks of exploration. As expected, rTg4510 mice exhibit profound impairments in hippocampal-dependent learning and memory tests, including contextual fear conditioning. However, rTg4510 mice also display an abnormal hyperexploratory phenotype in the open-field assay, elevated plus maze, light-dark exploration, and cued fear conditioning, indicative of amygdala dysfunction. Furthermore, significant tau burden is detected in the amygdala of both rTg4510 mice and human FTDP-17 patients, suggesting that the rTg4510 mouse model recapitulates the behavioral disturbances and neurodegeneration of the amygdala characteristic of FTDP-17.

KEYWORDS:

Amygdala; Frontotemporal dementia; Neurodegeneration; Tau; Tauopathy

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