What question did this study set out to answer?

To determine whether Alzheimer disease pathogenesis is associated with metabolic dysregulation in brain transmethylation and polyamine biochemical pathways.

January 24, 2020PLoS MedicineOpen Access

Dysregulation of multiple metabolic networks related to brain transmethylation and polyamine pathways in Alzheimer disease: A targeted metabolomic and transcriptomic study

View Full Paper

Ask AI

Bookmark

Authors

UMUma V. Mahajan VVVijay R. Varma MGMichael Griswold

Discussion

Member takes

Overview

Cross-sectional metabolomic and transcriptomic study uncovers widespread dysregulation of transmethylation and polyamine networks in Alzheimer disease, indicating severe metabolic vulnerability.

Key Points

To determine whether Alzheimer disease pathogenesis is associated with metabolic dysregulation in brain transmethylation and polyamine biochemical pathways.
Quantified 26 brain tissue metabolites using capillary electrophoresis-mass spectrometry in the inferior temporal gyrus and middle frontal gyrus of postmortem samples from the Baltimore Longitudinal Study of Aging (AD: n = 17, asymptomatic AD: n = 13, control: n = 13; 37.2% female; mean age 86.1 ± 9.8 years).
Evaluated mRNA expression of 71 pathway-related enzyme-coding genes across Gene Expression Omnibus datasets in the entorhinal cortex (AD: n = 25, control: n = 52) and hippocampus (AD: n = 29, control: n = 56).
Metabolite levels in the inferior temporal gyrus significantly correlated with CERAD and Braak scores, exhibiting increased S-adenosyl methionine (p = 0.005), cysteine (p < 0.001), reduced glutathione (p < 0.001), and spermidine (p = 0.004) in AD.
AD brains demonstrated significant reductions in choline (p = 0.003), N-acetyl glutamate (p < 0.001), N-acetyl aspartate (p = 0.002), and gamma-amino-butyric acid (p < 0.001).
Transcriptomic analyses confirmed significant alterations in gene expression levels of key enzymatic regulators governing transmethylation and polyamine synthesis and catabolism.

Cite This Study

Mahajan et al. (2020) studied this question.

synapsesocial.com/papers/6a86ceb348ef9afcd2a2413a https://doi.org/10.1371/journal.pmed.1003012

View Full Paper

Ask AI

Bookmark

January 24, 2020PLoS MedicineOpen Access

Dysregulation of multiple metabolic networks related to brain transmethylation and polyamine pathways in Alzheimer disease: A targeted metabolomic and transcriptomic study

View Full Paper

Ask AI

Bookmark

Authors

UMUma V. Mahajan VVVijay R. Varma MGMichael Griswold

Discussion

Member takes

Overview

Cross-sectional metabolomic and transcriptomic study uncovers widespread dysregulation of transmethylation and polyamine networks in Alzheimer disease, indicating severe metabolic vulnerability.

Key Points

To determine whether Alzheimer disease pathogenesis is associated with metabolic dysregulation in brain transmethylation and polyamine biochemical pathways.
Quantified 26 brain tissue metabolites using capillary electrophoresis-mass spectrometry in the inferior temporal gyrus and middle frontal gyrus of postmortem samples from the Baltimore Longitudinal Study of Aging (AD: n = 17, asymptomatic AD: n = 13, control: n = 13; 37.2% female; mean age 86.1 ± 9.8 years).
Evaluated mRNA expression of 71 pathway-related enzyme-coding genes across Gene Expression Omnibus datasets in the entorhinal cortex (AD: n = 25, control: n = 52) and hippocampus (AD: n = 29, control: n = 56).
Metabolite levels in the inferior temporal gyrus significantly correlated with CERAD and Braak scores, exhibiting increased S-adenosyl methionine (p = 0.005), cysteine (p < 0.001), reduced glutathione (p < 0.001), and spermidine (p = 0.004) in AD.
AD brains demonstrated significant reductions in choline (p = 0.003), N-acetyl glutamate (p < 0.001), N-acetyl aspartate (p = 0.002), and gamma-amino-butyric acid (p < 0.001).
Transcriptomic analyses confirmed significant alterations in gene expression levels of key enzymatic regulators governing transmethylation and polyamine synthesis and catabolism.

Cite This Study

Mahajan et al. (2020) studied this question.

synapsesocial.com/papers/6a86ceb348ef9afcd2a2413a https://doi.org/10.1371/journal.pmed.1003012

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

View Full Paper

Ask AI

Bookmark