Presentation Details
| Omics profiles of olfaction in aging and diseases Qu Tian, Luigi Ferrucci. National Institute on Aging, Baltimore, MD, USA |
Abstract
Olfaction deteriorates during aging, and olfactory deficit is an early sign of cognitive decline and neurodegenerative diseases. However, factors contributing to the loss of olfaction and the biological underpinnings of why olfaction serves as an early indicator of aging and diseases remain unclear. Potential mechanisms, such as lipid metabolism, immune responses, and diet, may be reflected in blood biomarkers. This talk focuses on omics markers of olfaction using the Baltimore Longitudinal Study of Aging data and discusses future directions and opportunities. Plasma lipid metabolites, assayed via FIA- and LC-mass spectrometry, were analyzed as six lipid classes. Plasma proteomics were assayed via the SomaScan 7k platform. Data was collected between 2015 and March 2020, before the COVID pandemic. From multivariable linear regression after adjusting for age, sex, and race, very long-chain(C22+) and long-chain(C14-C20) sphingomyelins and glycosylceramides were positively associated with olfaction (all p<0.05)(n=656). Very long-chain sphingomyelins and glycosylceramides attenuated and mediated the associations between olfaction and cognitive and physical functions (Δβ:10-26%). Of 7268 proteins examined, 21 proteins were associated with olfaction (p<0.005)(n=380). Top-ranked proteins were involved in the regulation of epithelial cells (CFTR, CRTP1), inflammation and immune responses (S100A11, CRTP1, Calgranulin A), endothelial cells (ROBO4), motor neurons (LMO4), mitosis (UBX2B), and mitochondrial function (PRR16). The identification of plasma omics markers may shed light on the contributing factors of olfaction loss and explain its connection to aging phenotypes and diseases. Future omics studies involving larger samples and longitudinal data are warranted to provide additional mechanistic insights.
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No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.