Effect of olfactory bulb pathology on olfactory function in normal aging

• Published in: Brain pathology (Zurich, Switzerland) Vol. 32; no. 5; pp. e13075 - n/a
• Main Authors: Tremblay, Cécilia, Serrano, Geidy E., Intorcia, Anthony J., Sue, Lucia I., Wilson, Jeffrey R., Adler, Charles H., Shill, Holly A., Driver‐Dunckley, Erika, Mehta, Shyamal H., Beach, Thomas G.
• Format: Journal Article
• Language: English
• Published: Switzerland John Wiley & Sons, Inc 01.09.2022; John Wiley and Sons Inc
• Subjects: Age; Aged; Aging; alpha-Synuclein - metabolism; Alzheimer Disease - pathology; Alzheimer's disease; Amyloid; Amyloid beta-Peptides - metabolism; amyloid β; Autopsies; Autopsy; Basal ganglia; Brain; Central nervous system diseases; Dementia; Dementia disorders; Humans; Letter to the Editor; Letters to the Editor; Lewy body disease; Medical research; Medicine, Experimental; Movement disorders; Nervous system diseases; Neurodegenerative diseases; Olfaction; Olfactory bulb; Olfactory Bulb - metabolism; Olfactory discrimination; Parkinson's disease; Pathology; Performance prediction; Smell; Synuclein; tau; Tau protein; tau Proteins - metabolism; α‐synuclein; olfactory bulb; Lewy body disease; amyloid β; tau; aging; Alzheimer's disease; α-synuclein
• ISSN: 1015-6305; 1750-3639; 1750-3639
• DOI: 10.1111/bpa.13075

Decline of olfactory function is frequently observed in aging and is an early symptom of neurodegenerative diseases. As the olfactory bulb (OB) is one of the first regions involved by pathology and may represent an early disease stage, we specifically aimed to evaluate the contribution of OB pathology to olfactory decline in cognitively normal aged individuals without parkinsonism or dementia. This clinicopathological study correlates OB tau, amyloid β (Aβ) and α‐synuclein (αSyn) pathology densities and whole brain pathology load to olfactory identification function as measured with the University of Pennsylvania Smell Identification Test (UPSIT) and clinical data measured proximate to death in a large autopsy study including 138 cases considered non‐demented controls during life. Tau pathology was frequently observed in the OB (95% of cases), while both Aβ (27% of cases) and αSyn (20% of cases) OB pathologies were less commonly observed. A weak correlation was only observed between OB tau and olfactory performance, but when controlled for age, neither OB tau, Aβ or αSyn significantly predict olfactory performance. Moreover, whole brain tau and αSyn pathology loads predicted olfactory performance; however, only αSyn pathology loads survived age correction. In conclusion, OB tau pathology is frequently observed in normally aging individuals and increases with age but does not appear to independently contribute to age‐related olfactory impairment suggesting that further involvement of the brain seems necessary to contribute to age‐related olfactory decline. Findings of this clinicopathological correlative study suggest that olfactory bulb pathology is frequently observed in normally aging individuals and increases with age but does not appear to independently contribute to age‐related olfactory impairment.