Abstract
The sense of smell has been shown to deteriorate in patients with some neurodegenerative disorders. In Parkinson’s disease (PD) and Alzheimer’s disease (AD), decreased ability to smell is associated with early disease stages. Thus, olfactory neurons in the nose and olfactory bulb (OB) may provide a window into brain physiology and pathophysiology to address the pathogenesis of neurodegenerative diseases. Because nasal olfactory receptor neurons regenerate throughout life, the olfactory system offers a broad variety of cellular mechanisms that could be altered in AD, including odorant receptor expression, neurogenesis and neurodegeneration in the olfactory epithelium, axonal targeting to the OB, and synaptogenesis and neurogenesis in the OB. This review focuses on pathophysiological changes in the periphery of the olfactory system during the progression of AD in mice, highlighting how the olfactory epithelium and the OB are particularly sensitive to changes in proteins and enzymes involved in AD pathogenesis. Evidence reviewed here in the context of the emergence of other typical pathological changes in AD suggests that olfactory impairments could be used to understand the molecular mechanisms involved in the early phases of the pathology.
Highlights
The sense of smell makes an important and often underestimated contribution to our quality of life
This review has focused on Alzheimer’s disease (AD) pathophysiology relating to events taking place in the olfactory system at the early processing stages, in particular, the olfactory epithelium (OE) and olfactory bulb (OB) in mouse models of AD (Figure 3)
Changes occurring in the OE that lead to neurodegeneration seem to be cell autonomous and independent of plaque accumulation
Summary
The sense of smell makes an important and often underestimated contribution to our quality of life. It is the only sensory organ that has its primary neurons in direct contact with the external world: the olfactory receptor neurons (ORNs) in the nasal cavity. As an island of neurons in the sea of the external world, the OE is an outpost that can potentially inform our knowledge about the brain’s physiological and pathological status. In neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD), olfactory dysfunction appears relatively early compared to other symptoms (Doty, 2009, 2012; Hummel et al, 2017). The use of olfactory function as the sole predictor of the AD is limited (Velayudhan, 2015)
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