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Updated: Aug 26, 2025

Olfactory Assays for Mouse Models of Neurodegenerative Disease
Published on: August 25, 2014
Smell deficits in COVID-19 and possible links with Parkinson's disease
Aron Emmi1, Michele Sandre2, Andrea Porzionato3
1Institute of Human Anatomy, Department of Neuroscience, University of Padova, Padova, Italy; Parkinson and Movement Disorders Unit, Department of Neuroscience, Centre for Rare Neurological Diseases (ERN-RND), University of Padova, Padova, Italy; Center for Neurodegenerative Disease Research (CESNE), University of Padova, Padova, Italy.
Abstract:
Olfactory impairment is a common symptom in Coronavirus Disease 2019 (COVID-19), the disease caused by Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) infection. While other viruses, such as influenza viruses, may affect the ability to smell, loss of olfactory function is often smoother and associated to various degrees of nasal symptoms. In COVID-19, smell loss may appear also in absence of other symptoms, frequently with a sudden onset. However, despite great clinical interest in COVID-19 olfactory alterations, very little is known concerning the mechanisms underlying these phenomena. Moreover, olfactory dysfunction is observed in neurological conditions like Parkinson's disease (PD) and can precede motor onset by many years, suggesting that viral infections, like COVID-19, and regional inflammatory responses may trigger defective protein aggregation and subsequent neurodegeneration, potentially linking COVID-19 olfactory impairment to neurodegeneration. In the following chapter, we report the neurobiological and neuropathological underpinnings of olfactory impairments encountered in COVID-19 and discuss the implications of these findings in the context of neurodegenerative disorders, with particular regard to PD and alpha-synuclein pathology.
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