Olfactory memory is impaired in a triple transgenic model of Alzheimer disease

Olfactory memory dysfunctions were investigated in the triple-transgenic murine model of Alzheimer's disease (3× Tg-AD). In the social transmission of food preference test, 3× Tg-AD mice presented severe deficits in odor-based memory, without gross changes in general odor-ability. Aβ and tau immunoreactivity was not observed in the primary processing regions for odor, the olfactory bulbs (OBs), whereas marked immunostaining was present in the piriform, entorhinal, and orbitofrontal cortex, as well as in the hippocampus. Our results suggest that the impairment in olfactory-based information processing might arise from degenerative mechanisms mostly affecting higher cortical regions and limbic areas, such as the hippocampus.

• 3× Tg-AD mice present impairment in short- and long-term odor-based memory, without gross changes in general odor-ability.
• Aβ and tau immunoreactivity was not observed in the olfactory bulbs, whereas marked immunostaining was present in the piriform, entorhinal, and orbitofrontal cortex, as well as in the hippocampus.
• AD-related olfactory memory impairment stems from lesions in cortical and limbic structures rather than in the OB.