Defects in Tongue Papillae and Taste Sensation Indicate a Problem with Neurotrophic Support in Various Neurological Diseases

Author:

Gardiner John1,Barton Deborah2,May Vanslambrouck Jessica3,Braet Filip4,Hall David5,Marc Jan2,Overall Robyn2

Affiliation:

1. School of Biological Sciences, the University of Sydney, Australia,

2. School of Biological Sciences, the University of Sydney, Australia

3. Gene and Stem Cell Therapy program, Centenary Institute of Cancer Medicine and Cell Biology, the University of Sydney, Australia

4. Australian Key Centre for Microscopy and Microanalysis, the University of Sydney, Australia

5. Wycombe Clinic, Neutral Bay Australia

Abstract

Neurotrophic support of developing neurons by neurotrophins is of critical importance in the development of fungiform papillae and taste buds. A number of neurological disorders show a decrease or increase in fungiform papillae or taste sensation. These can be grouped into disorders with reduced papillae (Machado-Joseph disease, Stüve-Wiedemann syndrome, familial dysautonomia, dystonia musculorum, and Behçet's disease) and those with taste defects only (Alzheimer's disease, Huntington's disease, hereditary sensory and autonomic neuropathy type IV, and diabetes mellitus). In addition, Parkinson's disease results in increased taste sensation. Here, we hypothesize that the main problem in these disorders is either not enough or too much neurotrophic support. Proneurotrophic drugs such as some antidepressants and aldose reductase inhibitors may prove useful in the treatment of these sensory and central nervous system disorders. Similarly, antineurotrophic drugs may also be useful in Parkinson's disease. Here we show that the protein involved in familial dysautonomia, IKAP, localizes to keratin filaments in HeLa cells, suggesting a role for the keratin cytoskeleton in neurotrophic support. NEUROSCIENTIST 14(3):240–250, 2008. DOI: 10.1177/1073858407312382

Publisher

SAGE Publications

Subject

Neurology (clinical),General Neuroscience

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