Opportunity Information: Apply for RFA AG 18 009
The Novel Cell Non-autonomous Mechanisms of Aging (R01) funding opportunity (RFA-AG-18-009) is a National Institutes of Health (NIH) research grant program focused on uncovering how aging in one cell or tissue can drive aging changes in other cells and tissues through signals that travel or are communicated across the body. Instead of looking only at "cell-autonomous" aging processes (the damage and dysfunction that build up within an individual cell), this FOA emphasizes "cell non-autonomous" mechanisms, meaning the outward-facing signals and messengers produced by aging cells that influence other cells at a distance. The intent is to fund projects that go beyond describing correlations and move toward a deeper, mechanistic understanding of what these aging signals are, how they arise from cell-intrinsic aging, how they are released, how they move between cells or tissues, and how they ultimately trigger aging-related effects once they reach their targets. The bigger picture goal is to clarify how important these non-autonomous signaling pathways are for aging at the tissue, organ system, or whole-organism level, and to generate insights that could reshape how researchers think about aging as a coordinated, multi-tissue process rather than a set of isolated cellular events.
Scientifically, the FOA is centered on the full lifecycle of an aging signal. It encourages applicants to identify the nature of the signals (for example, secreted factors, metabolites, extracellular vesicles, inflammatory mediators, neuroendocrine cues, immune-derived signals, or other communicators), explain how cell-autonomous aging processes generate them (such as stress responses, proteostasis collapse, mitochondrial dysfunction, senescence-associated changes, or DNA damage responses), and then map how these signals exit cells and propagate through the organism (release mechanisms, circulation, synaptic or paracrine routes, transport through fluids, or relay via intermediary cell types). It also prioritizes understanding how recipient cells detect and respond to these cues, including the downstream pathways that translate an incoming message into functional decline, altered repair capacity, inflammatory activation, metabolic disruption, stem cell exhaustion, or other hallmarks associated with aging. In practical terms, the FOA is looking for projects that build a coherent mechanistic chain from source cell aging to signal production, signal dissemination, and target cell aging outcomes, ideally in ways that illuminate new biology and open the door to intervention strategies later on.
Administratively, this opportunity is a discretionary NIH grant using the R01 funding instrument, categorized under health research with CFDA number 93.866. The original closing date listed for this particular FOA was October 3, 2017, and the opportunity record shows an award ceiling of $250,000, with the creation date of April 25, 2017. (In NIH contexts, budgeting and the meaning of a "ceiling" can vary depending on how the FOA was structured and what costs are considered, but the listing indicates that $250,000 is a key cap associated with this announcement.) The expected number of awards is not specified in the provided source text.
Eligibility is broad and includes many types of organizations typically able to apply for NIH research support. Eligible applicants include state, county, and city or township governments; special district governments; independent school districts; public and state-controlled institutions of higher education; private institutions of higher education; nonprofit organizations both with and without 501(c)(3) status (as long as they are not institutions of higher education in the nonprofit category described); public housing authorities and Indian housing authorities; federally recognized Native American tribal governments; Native American tribal organizations that are not federally recognized tribal governments; for-profit organizations other than small businesses; small businesses; and other eligible entities. The FOA also explicitly highlights additional eligible applicant categories such as Alaska Native and Native Hawaiian Serving Institutions, Asian American Native American Pacific Islander Serving Institutions (AANAPISIs), Hispanic-serving Institutions, Historically Black Colleges and Universities (HBCUs), Tribally Controlled Colleges and Universities (TCCUs), faith-based or community-based organizations, eligible federal agencies, U.S. territories or possessions, regional organizations, tribal governments that are not federally recognized, and non-domestic (non-U.S.) entities (foreign organizations). This emphasis signals a deliberate openness to a wide range of institutional types, including minority-serving institutions and international organizations, as long as they meet NIH requirements for the mechanism and FOA.
Overall, the opportunity is designed to push the field toward a more integrated understanding of aging as a communicative process, where damage or dysfunction in one location can spread influence through defined molecular or cellular messages. A competitive application under this FOA would be expected to propose genuinely novel, mechanistic work that clarifies the identity and origin of non-autonomous aging signals, the routes by which they travel, and the causal pathways through which they induce aging phenotypes in distant targets, ultimately improving understanding of aging at the level of tissues, organ systems, and the whole organism.Apply for RFA AG 18 009
- The National Institutes of Health in the health sector is offering a public funding opportunity titled "Novel Cell Non-autonomous Mechanisms of Aging (R01)" and is now available to receive applicants.
- Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.866.
- This funding opportunity was created on 2017-04-25.
- Applicants must submit their applications by 2017-10-03. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- Each selected applicant is eligible to receive up to $250,000.00 in funding.
- Eligible applicants include: State governments, County governments, City or township governments, Special district governments, Independent school districts, Public and State controlled institutions of higher education, Native American tribal governments (Federally recognized), Public housing authorities/Indian housing authorities, Native American tribal organizations (other than Federally recognized tribal governments), Nonprofits having a 501 (c) (3) status with the IRS, other than institutions of higher education, Nonprofits that do not have a 501 (c) (3) status with the IRS, other than institutions of higher education, Private institutions of higher education, For-profit organizations other than small businesses, Small businesses, Others.
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FAQs: Novel Cell Non-autonomous Mechanisms of Aging (R01) - RFA-AG-18-009
What is this funding opportunity?
This is an NIH research grant opportunity titled "The Novel Cell Non-autonomous Mechanisms of Aging (R01)" under FOA number RFA-AG-18-009. It uses the R01 funding mechanism and focuses on research that explains how aging in one cell or tissue can drive aging-related changes in other cells and tissues through signals communicated across the body.
What does "cell non-autonomous mechanisms of aging" mean in this FOA?
In this FOA, "cell non-autonomous" refers to aging effects that are driven by signals produced by aging cells that influence other cells at a distance. The emphasis is on outward-facing messengers (signals) released by a source cell or tissue that travel or are relayed to recipient cells, where they trigger aging-related outcomes.
How is this different from "cell-autonomous" aging research?
Cell-autonomous aging research focuses on damage and dysfunction that build up within an individual cell. This FOA is specifically interested in how cell-intrinsic aging processes generate signals that then affect other cells and tissues, making aging a coordinated, multi-tissue process rather than only a set of isolated cellular events.
What is the main scientific goal of the FOA?
The goal is to move beyond correlations and build a mechanistic understanding of how aging signals are produced, released, transmitted, and received, and how they cause aging-related effects in target cells and tissues. The bigger-picture aim is to clarify how important these pathways are for aging at the tissue, organ-system, and whole-organism levels.
What kinds of projects does NIH want to fund under this FOA?
The FOA seeks projects that establish a coherent mechanistic chain linking: (1) source cell aging, to (2) signal production, to (3) signal dissemination across cells/tissues, and finally to (4) target cell detection and aging-related outcomes. Competitive projects are expected to be genuinely novel and mechanistic rather than descriptive.
What types of aging signals are of interest?
The FOA encourages identifying the nature of aging signals, which may include (examples provided): secreted factors, metabolites, extracellular vesicles, inflammatory mediators, neuroendocrine cues, immune-derived signals, or other communicators that can transmit aging influence between cells or tissues.
What does the FOA mean by studying the "full lifecycle" of an aging signal?
It means understanding the entire pathway from start to finish, including: what the signal is, how it arises from cell-autonomous aging processes, how it is released from the source cell, how it travels or is relayed through the organism, and how it triggers specific downstream effects once it reaches recipient cells.
What cell-intrinsic aging processes are described as possible sources of these signals?
The FOA lists examples of cell-autonomous aging processes that could generate non-autonomous signals, including stress responses, proteostasis collapse, mitochondrial dysfunction, senescence-associated changes, and DNA damage responses.
What routes of signal transmission does the FOA mention?
The FOA highlights multiple possible routes, including release mechanisms from cells, circulation, synaptic routes, paracrine routes, transport through bodily fluids, and relay via intermediary cell types.
What should applicants study in recipient (target) cells?
The FOA prioritizes understanding how recipient cells detect and respond to aging cues, including identifying downstream pathways that translate an incoming message into aging-related outcomes.
What aging-related outcomes in target tissues are relevant to this FOA?
Examples of outcomes mentioned include functional decline, altered repair capacity, inflammatory activation, metabolic disruption, stem cell exhaustion, and other hallmarks associated with aging.
Does the FOA encourage intervention-focused studies?
The FOA emphasizes mechanistic understanding, with the idea that clarifying these signaling chains could open the door to later intervention strategies. The focus, as described, is on discovering and explaining mechanisms rather than only proposing correlations.
What is the funding mechanism for this opportunity?
This opportunity uses the NIH R01 research grant mechanism.
What agency is offering this grant?
The funding opportunity is offered by the National Institutes of Health (NIH).
What is the CFDA number listed for this opportunity?
The CFDA number provided is 93.866.
What is the award ceiling shown in the opportunity record?
The opportunity record shows an award ceiling of $250,000. The description notes that in NIH contexts, budgeting and how a "ceiling" is applied can vary depending on the FOA structure and what costs are included, but $250,000 is presented as a key cap for this announcement.
When was this opportunity created and what was the original closing date?
The creation date listed is April 25, 2017, and the original closing date listed is October 3, 2017.
How many awards are expected?
The expected number of awards is not specified in the provided information.
Who is eligible to apply?
Eligibility is broad and includes many organization types commonly eligible for NIH research support. Eligible applicants include: state, county, and city or township governments; special district governments; independent school districts; public and state-controlled institutions of higher education; private institutions of higher education; nonprofit organizations with or without 501(c)(3) status (as described in the source); public housing authorities and Indian housing authorities; federally recognized Native American tribal governments; non-federally recognized tribal organizations; for-profit organizations (including small businesses and other-than-small businesses); and other eligible entities.
Are minority-serving institutions specifically included as eligible applicants?
Yes. The FOA explicitly highlights additional eligible applicant categories such as Alaska Native and Native Hawaiian Serving Institutions, AANAPISIs, Hispanic-serving Institutions, HBCUs, and TCCUs.
Are faith-based and community-based organizations eligible?
Yes. The FOA explicitly lists faith-based or community-based organizations among the highlighted eligible applicant categories.
Are federal agencies and U.S. territories mentioned as eligible?
Yes. The FOA explicitly highlights eligible federal agencies, U.S. territories or possessions, and regional organizations.
Are non-U.S. (foreign) organizations eligible to apply?
Yes. The FOA explicitly includes non-domestic (non-U.S.) entities (foreign organizations) among the highlighted eligible applicant categories.
What overall view of aging is this FOA trying to promote?
It promotes the idea that aging can be a communicative, coordinated process across tissues, where dysfunction in one location can influence other locations through defined molecular or cellular messages, rather than aging being only independent events within individual cells.
What would make an application competitive based on the description provided?
A competitive application would propose novel, mechanistic research that identifies non-autonomous aging signals, explains how they originate from cell-intrinsic aging, clarifies how they are released and transmitted across the organism, and demonstrates causal pathways by which they induce aging phenotypes in distant targets.
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