NIH funding to study cellular mechanisms of aging
Novel Cell Non-autonomous Mechanisms of Aging (RFA-AG-18-009): https://grants.nih.gov/grants/guide/rfa-files/RFA-AG-18-009.html
The distinction between cell autonomous and non-autonomous effects driving aging was originally motivated by studies of development where some cells have the autonomous ability to differentiate whereas other cells differentiate through signals from neighboring cells. In the past few decades, most studies on the molecular mechanisms of aging have focused on the events within cells (cell-autonomous aging). These studies have led to a quite comprehensive understanding of the cell autonomous mechanisms of aging, including changes in many genes, pathways, biomolecules and organelles involved in the aging process. A dominant hypothesis, supported by observations obtained in the past several decades, has been that the underlying cause of aging is the cell autonomous, time-dependent accumulation of intracellular damage to biomolecules, organelles and cells. However, it has become apparent in recent years that cell-autonomous mechanisms alone are inadequate to explain aging at a tissue or organismal level. In multicellular organisms, it would be hard to accept that cell autonomous changes would limit their impact only within the border of a cell without causing cell non-autonomous consequences that affect aging at a tissue or organismal level. In fact, some compelling evidence in recent years—including parabiosis, serum transfer, cell ablation and molecular mechanistic studies—suggests that cell non-autonomous mechanisms also play important roles in driving degenerative changes of aging that arise as a consequence of cell-autonomous aging. Although the damages and changes initially occur in specific cells and tissues, it seems that these initial changes are communicated to other cells, tissues, or organs and thereby impact the lifespan and healthspan of the organism. For most of these non-autonomous players, we still don’t know what they are, the circumstances under which cell autonomous aging causes their synthesis and/or release, and how they elicit aging processes upon reaching their target cells. This FOA aims to stimulate research on novel insights and better understanding of the cell non-autonomous signaling in aging and longevity.
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The key goal to be achieved under this FOA is the identification and characterization of cell non-autonomous aging signals communicated to other cells and their mechanism of action on target cells and tissues. With this FOA, we aim to better understand what the non-autonomous aging signals are, how they are generated, and how they elicit aging processes upon reaching their target cells. It might also be useful to characterize the mechanisms of release and transport of signals for non-autonomous aging as part of the application. However, signal release and transport should not be a focus of the application.
To be responsive to this FOA, applications may include the identification and characterization of these cell non-autonomous aging signals, their communication and interaction with other molecules and cells, their transportation, and their modes of action at their target sites or cells. Applicants are encouraged to collaborate with other researchers to leverage expertise, needed technologies and resources. Studies using human samples, animal models, tissue culture or other in vitro systems such as cultured organoids are all considered appropriate in response to this FOA, as long as the objective of the research is to understand novel cell non-autonomous mechanisms responsible for the communication between different cells or tissues in aging and longevity.
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- Higher Education Institutions
- Nonprofits Other Than Institutions of Higher Education
- For-Profit Organizations, including small businesses
- And more
Letter of Intent Due Date(s): September 3, 2017
Application Due Date(s): October 3, 2017, by 5:00 PM local time of applicant organization
Earliest Start Date: July 2018
FOA Expiration Date: October 4, 2017