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Loss of smelling is an early marker of aging and is associated with inflammation and DNA damage in C57BL6/J mice

ABSTRACT: Olfactory dysfunction (loss of the ability to detect odors) is a prevalent symptom and an early marker of age-related neurodegenerative diseases in humans, including Alzheimer’s Disease and Parkinson’s Disease. However, as olfactory dysfunction also is a common symptom of normal aging, it is important to identify associated behavioral and mechanistic changes that underlie olfactory dysfunction in nonpathological aging. In the present study, we systematically investigated age-related behavioral changes in four specific domains of olfaction and the molecular basis in C57BL6/J mice. Our results show that selective loss of odor discrimination is the earliest smelling behavioral change with aging, followed by a decline in odor sensitivity and identification. Compared to behavioral changes related with memory and motor functions, smelling loss is among one of the earliest biomarkers of aging. During aging, metabolites related with of oxidative stress, osmolytes and infection become dysregulated in the olfactory bulb, and G protein coupled receptor related signaling was significantly down regulated in olfactory bulb of aged mice. Poly ADP-ribosylation levels and protein expressions of DNA damage markers and inflammation increased significantly in the olfactory bulb of older mice in which a lower NAD+ level was also detected. Supplementation of NAD+ through NR in water improved longevity and partially enhanced olfaction in aged mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE204966 | GEO | 2026/05/21

REPOSITORIES: GEO

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Project description:Olfactory sensory neurons distinguish a large variety of odor molecules and direct the information through their axons to the olfactory bulb, the first site for the processing of olfactory information in the brain. Olfaction is very important for most mammals for the maintenance of a good quality of life. Accumulating evidences endorse that olfactory sensory decline is connected with neurodegenerative disorders including schizophrenia, depression, multiple sclerosis, Huntington's, Alzheimer's and Parkinson's diseases. For several decades, neuroanatomical, volumetric, and histological approaches have been the gold standard techniques employed to characterize the olfactory bulb functionality. Diagnosis and treatment of olfactory dysfunction remain significant health care challenges to society. Novel strategies and clues that assist in the identification of biomarker and drug development for aid in the prevention and cure of neurological diseases are necessary. However, little attention has been focused specifically on the molecular composition of the olfactory bulb from the perspective of proteomics. To this end, an in-depth mapping of the olfactory bulb proteome was carried out using high resolution tandem mass spectrometry, revealing a repertoire of 7,754 proteins. A large proportion of the identified proteins were predicted to be involved in diverse biological processes including signal transduction, metabolism, transport, olfaction and protein synthesis. Pathway analysis of the identified proteins shows that, these proteins are predominantly involved in metabolic and neural processes, chromatin modeling, and synaptic vesicle transport associated with neuronal transmission. In total, our study offers valuable understandings into the molecular composition of the human olfactory bulb proteome that could possibly help neuroscience community to understand the olfactory bulb better and open avenues for intervention strategies for olfactory dysfunction in the future.

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Loss of smelling is an early marker of aging and is associated with inflammation and DNA damage in C57BL6/J mice

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