Metabolomics

Dataset Information

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Neuronal Hyperactivity due to Loss of Inhibitory Tone in APOE4 Mice Lacking Alzheimer’s Disease-like Pathology


ABSTRACT: Metabolite profiling was performed on metabolites extracted from the entorhinal cortex and primary visual cortex of 14-15 month old APOE3/3, APOE3/4 and APOE4/4 mice. Metabolites were run on a TOF Mass Spectrometer using an ANP column. Initial analysis was done in an untargeted manner, and processing was done to determine the differentially expressed metabolites based on their mass and retention times. Further analysis was then performed to assign identities to the differentially expressed metabolites using a database of biologically-relevant metabolites whose standards had been run under identical conditions as the samples in the study.

INSTRUMENT(S): 6230 TOF LC/MS (Agilent)

SUBMITTER: Tal Nuriel 

PROVIDER: MTBLS530 | MetaboLights | 2017-09-05

REPOSITORIES: MetaboLights

Dataset's files

Source:
Action DRS
MTBLS530 Other
FILES Other
a_MTBLS530_NEG_mass_spectrometry.txt Txt
a_MTBLS530_POS_mass_spectrometry.txt Txt
i_Investigation.txt Txt
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Publications


The ε4 allele of apolipoprotein E (APOE) is the dominant genetic risk factor for late-onset Alzheimer's disease (AD). However, the reason APOE4 is associated with increased AD risk remains a source of debate. Neuronal hyperactivity is an early phenotype in both AD mouse models and in human AD, which may play a direct role in the pathogenesis of the disease. Here, we have identified an APOE4-associated hyperactivity phenotype in the brains of aged APOE mice using four complimentary techniques-fMR  ...[more]

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