@article{c8a444ee0caf4e7ba9811d23de48b7c2,
title = "Aerobic glycolysis in the human brain is associated with development and neotenous gene expression",
abstract = "Aerobic glycolysis (AG; i.e., nonoxidative metabolism of glucose despite the presence of abundant oxygen) accounts for 10%-12% of glucose used by the adult human brain. AG varies regionally in the resting state. Brain AG may support synaptic growth and remodeling; however, data supporting this hypothesis are sparse. Here, we report on investigations on the role of AG in the human brain. Meta-analysis of prior brain glucose and oxygen metabolism studies demonstrates that AG increases during childhood, precisely when synaptic growth rates are highest. In resting adult humans, AG correlates with the persistence of gene expression typical of infancy (transcriptional neoteny). In brain regions with the highest AG, we find increased gene expression related to synapse formation and growth. In contrast, regions high in oxidative glucose metabolism express genes related to mitochondria and synaptic transmission. Our results suggest that brain AG supports developmental processes, particularly those required for synapse formation and growth.",
author = "Goyal, {Manu S.} and Michael Hawrylycz and Miller, {Jeremy A.} and Snyder, {Abraham Z.} and Raichle, {Marcus E.}",
note = "Funding Information: We thank Matthew Glasser for providing a geodesically smoothed representation of human brain aerobic glycolysis on the brain surface. We are also grateful for the many thoughtful discussions that we had with Anish Mitra, Ben Shannon, and Ed Lein as well as the thoughtful comments provided by our anonymous reviewers. We thank the Allen Institute founders, Paul G. Allen and Jody Allen, for their vision, encouragement, and support. The Allen Human Brain Atlas was supported in part by award numbers 1C76HF15069-01-00 and 1C76HF19619-01-00 from the Department of Health and Human Services Health Resources and Services Administration. This work was supported by National Institutes of Health (P50 NS006833 to M.E.R. and A.Z.S.) and the National Institute of Neurologic Disorders and Stroke (P30 NS048056 to A.Z.S.). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health or the Department of Health and Human Services. ",
year = "2014",
month = jan,
day = "7",
doi = "10.1016/j.cmet.2013.11.020",
language = "English",
volume = "19",
pages = "49--57",
journal = "Cell metabolism",
issn = "1550-4131",
number = "1",
}