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- W3044286795 abstract "Abstract Alzheimer’s disease (AD) is a progressive and debilitating neurodegenerative disorder and one of the leading causes of death in the United States. Although amyloid plaques and fibrillary tangles are hallmarks of AD, research suggests that pathology associated with AD often begins 20 or more years before symptoms appear. Therefore, it is essential to identify early-stage biomarkers in those at risk for AD and age-related cognitive decline (ARCD) in order to develop preventative treatments. Here, we used an untargeted metabolomics analysis to define system-level alterations following cognitive decline in aged and APP/PS1 (AD) mice. At 6, 12, and 24 months of age, both control (Ctrl) and AD mice were tested in a 3-shock contextual fear conditioning (CFC) paradigm to assess memory decline. AD mice exhibited memory deficits across age and these memory deficits were also seen in naturally aged mice. Prefrontal cortex (PFC), hippocampus (HPC), and spleen were then collected and analyzed for metabolomic alterations. A number of significant pathways were altered between Ctrl and AD mice and naturally aged mice. By identifying systems-level alterations following ARCD and AD, these data could provide insights into disease mechanisms and advance the development of biomarker panels." @default.
- W3044286795 created "2020-07-29" @default.
- W3044286795 creator A5008685777 @default.
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- W3044286795 date "2020-07-22" @default.
- W3044286795 modified "2023-10-05" @default.
- W3044286795 title "Divergence in the metabolome between natural aging and Alzheimer’s disease" @default.
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- W3044286795 doi "https://doi.org/10.1038/s41598-020-68739-z" @default.
- W3044286795 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7376199" @default.
- W3044286795 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32699218" @default.
- W3044286795 hasPublicationYear "2020" @default.
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