Unveiling the biological substrates of glucose metabolic covariance in human brain

Brisbane Convention & Exhibition Centre 

Glucose metabolism is essential for providing the energetic supply that supports the neural dynamics vital for brain function. Abnormal glucose metabolism, such as hypo- and hypermetabolism, is frequently reported in patients with neurological diseases, including Alzheimer's disease and epilepsy. It has become clear that regional metabolic changes are not isolated incidents; rather, local inhibitory circuitry or diaschisis, due to connections from pathological regions, may also affect local metabolism. These remote impacts, which can be characterized by metabolic covariance networks (MCNs), have been found to be indicative of brain pathologies [1]. However, the biological substrates of such covariance-specifically, the basis on which this covariance emerges-remain to be elucidated. Based on multimodal imaging data from a group of temporal lobe epilepsy (TLE) patients, we explore the fundamental determinants of MCN, including intrinsic functional connectivity (FC), white matter pathways (structural connectivity, SC), morphometric similarity (structural covariance network, SCN), geometric proximity (Euclidean distance, ED), as well as neurochemical and genetic underpinnings.