(DOI: ).įunding: The author(s) received no specific funding for this work.Ĭompeting interests: The authors have declared that no competing interests exist.Īlzheimer’s disease (AD) is an age-related, degenerative brain disease characterized by progressive cognitive impairment and dementia with increasing deficiency in multiple cognitive domains including memory, executive functions and language. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: Data are available from the following: CSF metabolic profiles: NOESY experiment: (DOI: ) Blood metabolic profiles: CPMG experiment: and this information has been added to the manuscript. Received: JAccepted: ApPublished: May 10, 2021Ĭopyright: © 2021 Stojanovic et al. Ginsberg, Nathan S Kline Institute, UNITED STATES (2021) NMR analysis of the correlation of metabolic changes in blood and cerebrospinal fluid in Alzheimer model male and female mice. Metabolite changes observed in the APP/PS1 mouse model are the response to the mutation causing plaque formation, not the cause for the plaque suggesting that they are less relevant in the context of early treatment and prevention then the metabolic changes observed only in humans.Ĭitation: Stojanovic F, Taktek M, Khieu NH, Huang J, Jiang S, Rennie K, et al. Metabolites concentration and correlation changes in CSF, blood and across the blood brain barrier determined in this work are affected by the production of amyloid plaque. Using our novel method for analysis of correlation and mathematical ranking of significant correlations between metabolites in CSF and blood, we have explored changes in metabolite correlation and connectedness in APP/PS1 and wild type mice. Analysis of metabolic profile of cerebrospinal fluid (CSF) and blood of APP/PS1 mouse model can provide information about metabolic changes in these body fluids caused by Aβ accumulation. The mouse model APP/PS1 expresses a mutant amyloid precursor protein resulting in early Amyloid β (Aβ) accumulation as well as many resulting physiological changes including changes in metabolic profile and metabolism. However, with analysis performed at the late stages of the disease it is not possible to distinguish causes and consequence. Metabolomics studies of body fluids as well as brain tissues have shown major changes in metabolic profiles of Alzheimer’s patients. The development of effective therapies as well as early, molecular diagnosis of Alzheimer’s disease is impeded by the lack of understanding of the underlying pathological mechanisms.
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