"The loss of smell or olfactory dysfunction has been known for more than a decade as an early sign of several neurodegenerative diseases, but we have never been able to link it to a pathological entity that is measurable over time," said Richard Doty, PhD, Professor and Director of Penn's Smell and Taste Center, who is also the team leader of the study. "By tying decrements in the ability to smell to the presence of key disease proteins, such as tau, we may well be able to assess the degree of progression of selected elements of Alzheimer's disease and related disorders by scores on quantitative smell tests."
A total of ten mice were evaluated in this experiment five mice that were genetically engineered to be a model for human Alzheimer's and Parkinson's disease, and five normal control mice that do not overexpress tau proteins. Olfactory dysfunction was evaluated by measuring the amount of time the mice spent investigating unfamiliar odors, such as peppermint or vanillin. Unlike normal mice, those with smell deficits do not spend much time investigating such odors, and do not show a preference for "novel" odors over "familiar" odors.
The results of the Penn study showed that only the control mice, with no excess of tau proteins, expressed an interest in new odors, indicating a normal sense of smell. The mice that had excess in tau protei
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Contact: David March
david.march@uphs.upenn.edu
215-615-3353
University of Pennsylvania School of Medicine
11-Mar-2004