Affiliations: [a]
The University of Texas at San Antonio, Department of Biology, One UTSA Circle, San Antonio, TX, USA
| [b]
The University of Texas at San Antonio, Neurosciences Institute, One UTSA Circle, San Antonio, TX, USA
Correspondence:
[*]
Correspondence to: Lindsey J. Macpherson, PhD, The University of Texas at San Antonio, Department of Biology, One UTSA Circle, San Antonio, Texas 78249, USA. Tel.: +1 210 458 7845; E-mail: [email protected].
Abstract: Background:Previous studies indicate that taste dysfunction occurs early in the development of Alzheimer’s disease. It is debatable whether the deficit in taste is due primarily to peripheral sensory mechanisms or to central processing, or a combination of the two. Objective:The aim of our current study is to combine behavior and histological data in APP/PS1 transgenic mice to determine whether APP/PS1 transgenic mice show deficits in unconditioned taste preference and avoidance behaviors and whether taste impairments are due to defects in the peripheral taste system and/or problems with central processing of taste information. Methods:The APP/PS1 transgenic mutant mice were used as a model of Alzheimer’s disease. We employed a brief-access gustometer test to assess immediate orosensory taste responses of APP/PS1 mice. We used immunohistochemistry to examine tongue, gustatory ganglion, and brain tissues to determine a cytological basis for behavioral deficits. Results:There is a significant, selective reduction of bitter taste sensitivity in APP/PS1 mice. These mice also have a loss of TRPM5-expressing taste receptor cells in the circumvallate papillae of the tongue. While we observed no overt loss of neuron cell bodies within the primary gustatory sensory neurons, degeneration of the neurons’ peripheral axons innervating the taste bud may play a role in the observed loss of TRPM5-expressing taste receptor cells. Conclusion:This data supports a potential role for peripheral taste dysfunction in AD through the selective loss of taste receptor cells. Further study is necessary to delineate the mechanisms and pathological significance of this deficit in AD.
