Affiliations: [a] Centre for Neuroscience Studies, Queen’s University, Kingston, Ontario, ON, Canada
| [b] Department of Biomedical and Molecular Sciences, Queen’s University, Kingston, Ontario, ON, Canada
Correspondence:
[*]
Correspondence to: Michael Kawaja, Centre for Neuroscience Studies, Queen’s University, Kingston, Ontario
K7L 3N6, OA, Canada. Tel.: +1 613 328 6349; E-mail: [email protected].
Abstract: Alzheimer’s disease is the most common cause of dementia, and it is one of the leading causes of death globally. Identification and validation of biomarkers that herald the onset and progression of Alzheimer’s disease is of paramount importance for early reliable diagnosis and effective pharmacological therapy commencement. A substantial body of evidence has emerged demonstrating that olfactory dysfunction is a preclinical symptom of neurodegenerative diseases including Alzheimer’s disease. While a correlation between olfactory dysfunction and Alzheimer’s disease onset and progression in humans exists, the mechanism underlying this relationship remains unknown. The aim of this article is to review the current state of knowledge regarding the range of potential factors that may contribute to the development of Alzheimer’s disease-related olfactory dysfunction. This review predominantly focuses on genetic mutations associated with Alzheimer’s disease including amyloid-β protein precursor, presenilin 1 and 2, and apolipoprotein E mutations, that may (in varying ways) drive the cellular events that lead to and sustain olfactory dysfunction.
Keywords: Alzheimer’s disease, amyloid-beta protein precursor, Apolipoprotein E, impaired olfaction, presenilins
