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Innervation in human taste buds and its decrease in Alzheimer's disease patients
M Yamagishi1, S Takami, T V Getchell
1Department of Surgery, University of Kentucky College of Medicine, Lexington, USA.
Acta Oto-Laryngologica
|September 1, 1995
Summary
Alzheimer's disease (AD) patients show significantly reduced taste bud innervation, particularly using the protein gene product 9.5 (PGP 9.5) marker. This decreased nerve supply may contribute to the diminished sense of taste in individuals with AD.
Area of Science:
- Neuroscience
- Histology
- Pathology
Background:
- Taste disorders are common in Alzheimer's disease (AD).
- The specific changes in taste bud innervation in AD are not well understood.
- Immunohistochemistry offers a method to study neuronal markers in taste buds.
Purpose of the Study:
- To investigate the innervation of human foliate and circumvallate papillae taste buds.
- To compare taste bud innervation between Alzheimer's disease (AD) patients and controls.
- To identify suitable neuronal markers for studying taste bud innervation.
Main Methods:
- Immunohistochemical analysis using antisera for protein gene product 9.5 (PGP 9.5), neuron-specific enolase (NSE), tyrosine hydroxylase (TH), dopamine-beta hydroxylase (DbetaH), and calcitonin gene-related peptide (CGRP).
- Studied human foliate and circumvallate papillae from AD and control (ADC) patients.
- Quantified intragemmal nerve fibers using PGP 9.5.
Main Results:
- PGP 9.5 was the most effective marker for identifying intragemmal nerve fibers in taste buds.
- NSE immunoreactivity was found in both nerve fibers and taste bud cells.
- TH- and DbetaH-immunoreactive fibers were absent; CGRP-immunoreactive fibers were rare.
- A significant decrease in PGP 9.5-immunoreactive nerve fibers was observed in the taste buds of AD patients compared to controls.
Conclusions:
- PGP 9.5 is a reliable marker for human taste bud innervation.
- Alzheimer's disease is associated with a significant reduction in taste bud nerve fibers.
- Reduced innervation may contribute to the chemosensory deficits observed in Alzheimer's disease.