Regulation of survival, growth, and metabolism by neuronal mTOR.

Stacy A Hussong, Raquel Burbank Roberts, Jonathan J Halloran, Stephen F Hernandez, Candice E Van Skike, Angela O Dorigatti, Nicholas DeRosa, Michael E Walsh, Vanessa Y Soto, Daniel A Pulliam, Holly Van Remmen, Steven N Austad, Veronica Galvan

Department of Biochemistry and Physiology, at the University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. · pubmed

Paper

Abstract

Reducing activity of the mechanistic/mammalian target of rapamycin (mTOR) with rapamycin extends lifespan and healthspan in many species. The mechanisms by which mTOR regulates lifespan and healthspan, however, are still unknown. Understanding how mTOR signaling in different cell types regulates lifespan and aspects of healthspan is urgently needed if we are to harness the potential individual and societal benefits of healthspan extension by mTOR attenuation. mTOR kinase can form two complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The regulatory associated protein of mTOR (Raptor) is required for the assembly of mTORC1, the primary target of rapamycin. To define the role of mTORC1 and mTORC2 signaling during development in the regulation of healthspan we either ablated or reduced expression of Rptor (Raptor) or Mtor (mTOR) in neurons of mice. Developmental knock-down of Mtor (mTOR

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the role of mTOR signaling in neurons and its impact on lifespan and healthspan. This research is relevant as it addresses the underlying mechanisms of aging and potential interventions for lifespan extension through mTOR modulation.

Author of this paper? Send a correction.