Aging is associated with a modality-specific decline in taste
Biorxiv : the Preprint Server for Biology
|February 14, 2024
Summary
Aging impairs taste in fruit flies, specifically sugar detection, mirroring Alzheimer's Disease (AD) effects. This suggests localized neural changes, not widespread neurodegeneration, underlie these sensory deficits.
Area of Science:
- Neuroscience
- Gerontology
- Molecular Biology
Background:
- Chemosensory deficits are linked to aging and neurodegenerative diseases like Alzheimer's Disease (AD).
- Understanding these deficits offers insights into aging and neurodegeneration mechanisms.
- The fruit fly, *Drosophila melanogaster*, serves as a model to study aging and neurodegeneration, but taste aspects remain under-explored.
Approach:
- Compared aged and young flies' responses to different tastants (sugars, fatty acids).
- Used genetic manipulation to express amyloid-beta peptide in specific taste neurons.
- Performed functional imaging of gustatory axon terminals and analyzed gene expression in taste neurons.
Key Points:
- Aging caused modality-specific taste deficits, impairing sugar response but not fatty acid response.
- Amyloid-beta expression in sweet-sensing neurons mimicked aging-related deficits, localizing the issue to gustatory neurons.
- Transcriptome analysis revealed age-related gene expression changes, including reduced odorant-binding proteins in sugar-sensing neurons.
Conclusions:
- Age-related taste decline appears localized to gustatory neurons and may involve signaling pathway-specific changes.
- Amyloid-beta expression leads to reduced innervation in the taste center, suggesting distinct mechanisms for taste deficits in aging vs. AD models.
- This study establishes a *Drosophila* model for investigating cellular deficits in neural function related to aging and AD.
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