Aging is associated with a modality-specific decline in taste.

Deficits in chemosensory processing are associated with healthy aging, as well as numerous neurodegenerative disorders, including Alzheimer's disease (AD). The fruit fly, , is a powerful model for studying chemosensation, aging, and aging-related pathologies, yet the effects of aging and neurodegeneration on taste function remain largely unexplored. Aging impaired response to sugars, but not medium-chain fatty acids that are sensed by a shared population of neurons. Selective expression of the human amyloid beta (Aβ) peptide phenocopied the effects of aging. Functional imaging of gustatory axon terminals revealed reduced response to sugar, but not fatty acids. Axonal innervation of the fly taste center was largely intact in aged flies; however, axonal innervation was reduced upon expression of Aβ. A comparison of transcript expression within the sugar-sensing taste neurons revealed age-related changes in 66 genes. Together, these findings suggest that different mechanisms underly taste deficits in aged and AD model flies.