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Age-related olfactory dysfunction: cellular and molecular characterization in the rat.
David B Conley1, Alan M Robinson, Michael J Shinners
1Department of Otolaryngology-Head and Neck Surgery, Northwestern University Medical School, Chicago, Illinois 60611, USA.
American Journal of Rhinology
|July 17, 2003
Summary
Aging increases olfactory receptor neuron (ORN) cell death, contributing to age-related olfactory dysfunction. This study found increased apoptosis-related gene expression and a higher apoptotic index in aged rats, suggesting cell death, not reduced proliferation, underlies olfactory decline.
Area of Science:
- Neuroscience
- Cell Biology
- Aging Research
Background:
- Olfactory receptor neurons (ORNs) naturally undergo apoptosis.
- ORNs are susceptible to environmental injury.
- Mammals typically replace ORNs throughout life, but this fails in aging humans, leading to olfactory dysfunction.
Purpose of the Study:
- To investigate whether age-related olfactory dysfunction stems from decreased neuronal proliferation or increased ORN cell death.
- To compare age-related changes with those induced by injury.
Main Methods:
- Assessed apoptosis-related gene expression (Bax, Bcl-xL, procaspase-3) in rat olfactory epithelium (OE) using ribonuclease protection assay.
- Quantified ORN apoptosis (apoptotic index) via terminal deoxynucleotide transferase end labeling assay in young, old, and bulbectomized rats.
Main Results:
- Aged rats showed increased expression of apoptosis-related genes compared to young rats.
- Bulbectomy (ORN injury model) induced a more pronounced increase in these genes.
- Both aging and bulbectomy significantly increased the apoptotic index of ORNs.
Conclusions:
- Aging and injury induce similar changes in the olfactory epithelium.
- Increased ORN cell death is a significant factor in age-related olfactory dysfunction.