Omics‐derived biological modules reflect metabolic brain changes in Alzheimer's disease

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, w...

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Veröffentlicht in:Alzheimer's & dementia 2024-10, Vol.20 (10), p.6709-6721
Hauptverfasser: Povala, Guilherme, De Bastiani, Marco Antônio, Bellaver, Bruna, Ferreira, Pamela C. L., Ferrari‐Souza, João Pedro, Lussier, Firoza Z., Souza, Diogo O., Rosa‐Neto, Pedro, Pascoal, Tharick A., Zatt, Bruno, Zimmer, Eduardo R.
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Sprache:eng
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Zusammenfassung: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 
ISSN:1552-5260
1552-5279
1552-5279
DOI:10.1002/alz.14095