The olfactory vector hypothesis of neurodegenerative disease: Is it viable?

Environmental agents, including viruses, prions, and toxins, have been implicated in the cause of a number of neurodegenerative diseases, most notably Alzheimer's and Parkinson's diseases. The presence of smell loss and the pathological involvement of the olfactory pathways in the formativ...

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Bibliographic Details
Published in:Annals of neurology 2008-01, Vol.63 (1), p.7-15
Main Author: Doty, Richard L.
Format: Article
Language:English
Subjects:
Alzheimer Disease - chemically induced
Alzheimer Disease - physiopathology
Alzheimer Disease - virology
Animals
Axonal Transport
Biological and medical sciences
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Disease Progression
Dyskinesia, Drug-Induced - physiopathology
Hazardous Substances - toxicity
Humans
Medical sciences
Neurodegenerative Diseases - chemically induced
Neurodegenerative Diseases - physiopathology
Neurodegenerative Diseases - virology
Neurology
Olfaction Disorders - chemically induced
Olfaction Disorders - physiopathology
Olfaction Disorders - virology
Olfactory Mucosa - drug effects
Olfactory Mucosa - physiopathology
Olfactory Mucosa - virology
Parkinson Disease - physiopathology
Parkinson Disease - virology
Virus Diseases - physiopathology
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Summary:Environmental agents, including viruses, prions, and toxins, have been implicated in the cause of a number of neurodegenerative diseases, most notably Alzheimer's and Parkinson's diseases. The presence of smell loss and the pathological involvement of the olfactory pathways in the formative stages of Alzheimer's and Parkinson's diseases, together with evidence that xenobiotics, some epidemiologically linked to these diseases, can readily enter the brain via the olfactory mucosa, have led to the hypothesis that Alzheimer's and Parkinson's diseases may be caused or catalyzed by agents that enter the brain via this route. Evidence for and against this concept, the “olfactory vector hypothesis,” is addressed in this review. Ann Neurol 2008;63:7–15
ISSN:0364-5134
1531-8249
DOI:10.1002/ana.21327