Abstract
INTRODUCTION
Brain glucose hypometabolism, indexed by the fluorodeoxyglucose positron emission tomography ([18F]FDG-PET) imaging, is a metabolic signature of Alzheimer’s disease (AD). However, the underlying biological pathways involved in these metabolic changes remain elusive.
METHODS
Here, we integrated [18F]FDG-PET images with blood and hippocampal transcriptomic data from cognitively unimpaired (CU, n = 445) and cognitively impaired (CI, n = 749) individuals using modular dimension reduction techniques and voxel-wise linear regression analysis.
RESULTS
Our results showed that multiple transcriptomic modules are associated with brain [18F]FDG-PET metabolism, with the top hits being a protein serine/threonine kinase activity gene cluster (peak-t
(223)
= 4.86, P value < 0.001) and zinc-finger–related regulatory units (peak-t
(223)
= 3.90, P value < 0.001).
DISCUSSION
By integrating transcriptomics with PET imaging data, we identified that serine/threonine kinase activity–associated genes and zinc-finger–related regulatory units are highly associated with brain metabolic changes in AD.
Highlights
We conducted an integrated analysis of system-based transcriptomics and fluorodeoxyglucose positron emission tomography ([18F]FDG-PET) at the voxel level in Alzheimer’s disease (AD).
The biological process of serine/threonine kinase activity was the most associated with [18F]FDG-PET in the AD brain.
Serine/threonine kinase activity alterations are associated with brain vulnerable regions in AD [18F]FDG-PET.
Zinc-finger transcription factor targets were associated with AD brain [18F]FDG-PET metabolism.
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This post is Copyright: Guilherme Povala,
Marco Antônio De Bastiani,
Bruna Bellaver,
Pamela C. L. Ferreira,
João Pedro Ferrari‐Souza,
Firoza Z. Lussier,
Diogo O. Souza,
Pedro Rosa‐Neto,
Tharick A. Pascoal,
Bruno Zatt,
Eduardo R. Zimmer,
for the Alzheimer’s Disease Neuroimaging Initiative | August 14, 2024