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Article type: Review Article
Authors: Parvand, Mahraza | Rankin, Catharine H.a; b; *
Affiliations: [a] Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC, Canada | [b] Department of Psychology, University of British Columbia, Vancouver, BC, Canada
Correspondence: [*] Correspondence to: Catharine H. Rankin, PhD, Department of Psychology, 2136 West Mall, Vancouver, BC, V6T 1Z4, Canada. Tel.: +1 604 822 5449; Fax: +1 604 822 6923; E-mail: [email protected].
Abstract: As we age, our olfactory function declines. In addition to occurring in normal aging, more rapid decrement of olfactory decline has been associated with several neurodegenerative diseases including Alzheimer’s disease (AD) and Parkinson’s disease (PD). It has been argued that since olfactory deficits occur less frequently or are absent in diseases such as progressive supranuclear palsy, corticobasal degeneration, and multiple system atrophy, olfactory deficits can be used for differential diagnoses of AD and PD. The purpose of this review is to provide a survey of current knowledge about the molecular bases and differential patterns of olfactory deficits present in normal aging, AD, and PD. As substantial research has been conducted in this area, the majority of the content of this review focuses on articles published in the past decade. We hypothesize that olfactory deficits in normal aging, AD, and PD may have different underlying causes, and propose the use of model organisms with small, tractable nervous systems and/or easy to manipulate genomes to further investigate the cellular mechanisms responsible for these deficits.
Keywords: Aging, Alzheimer’s disease, olfaction, Parkinson’s disease, Smell
DOI: 10.3233/JAD-190636
Journal: Journal of Alzheimer's Disease, vol. 73, no. 1, pp. 1-21, 2020
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