Opportunity Information: Apply for RFA AG 17 053
The National Institutes of Health (NIH) funding opportunity titled "Human Cell Biology of Genetic Variants in Alzheimer's Disease (R01)" (Funding Opportunity Number RFA-AG-17-053; CFDA 93.866) is a discretionary research grant aimed at clarifying how specific human genetic variants linked to Alzheimer's disease (AD) actually influence cell behavior in the brain. The central idea is to move beyond statistical associations found in large human genetics studies and instead demonstrate causal, functional connections between AD-associated variants and measurable biological changes in human neural cells. By doing this, the program seeks to sharpen understanding of AD disease mechanisms and help identify molecular targets that could be relevant for therapy development.
The scientific focus is on establishing genotype-phenotype relationships for variants suspected of changing AD risk. These variants often come from genome-wide association studies (GWAS) and genome sequencing efforts that can pinpoint regions of the genome correlated with disease risk but do not automatically reveal which gene is affected, what direction the effect goes in, or what cellular pathway is disrupted. This FOA emphasizes functional follow-up, meaning applicants are expected to test how these variants alter molecular and cellular phenotypes in relevant human cell types rather than relying only on computational predictions or non-human model systems.
A key requirement of the approach is the use of human induced pluripotent stem cells (iPSCs) or other human cell reprogramming methods to generate neural cells for experiments. In practical terms, this typically means deriving or engineering human cell lines that carry specific AD-linked genetic variants and differentiating them into neurons and/or glial cell types (such as astrocytes, microglia-like cells, or oligodendrocytes) so investigators can observe variant-driven effects in a human cellular context. The underlying rationale is that AD risk variants may exert their effects in ways that are difficult to capture in animal models or immortalized cell lines, and that human reprogrammed neural systems can better reflect the biology of human brain cells, including relevant gene regulation and disease-relevant pathways.
The outcomes NIH is looking for are experimentally supported links between AD genetics and cellular mechanisms. That can include molecular phenotypes (for example, altered gene expression programs, splicing changes, epigenetic states, protein levels, or pathway activation) as well as biological cell phenotypes (for example, changes in neuronal function, synaptic biology, cellular stress responses, inflammatory signaling in glia, protein processing and trafficking, lipid metabolism, or other cell behaviors plausibly connected to AD etiology). The FOA frames these results as a way to gain greater insight into molecular targets contributing to the origins and progression of Alzheimer's disease, effectively building a bridge between human genetic discovery and mechanistic biology in human neural cells.
This opportunity uses the NIH R01 mechanism, meaning it is structured to support substantial, hypothesis-driven research projects with clearly defined aims, rigorous experimental design, and strong justification for the chosen models and readouts. The awarding agency is NIH, and the funding activity category is Health. The listed original closing date for the opportunity was February 10, 2017, and the opportunity record indicates a creation date of October 21, 2016. Award ceiling and expected number of awards are not specified in the provided source data.
Eligibility is broad and includes many types of U.S. organizations and, notably, certain non-U.S. entities as well. Eligible applicants include state, county, city, township, and special district governments; independent school districts; public and state-controlled institutions of higher education; private institutions of higher education; federally recognized Native American tribal governments; other Native American tribal organizations; public housing authorities/Indian housing authorities; nonprofit organizations with or without 501(c)(3) status (other than institutions of higher education); for-profit organizations other than small businesses; small businesses; and other unspecified eligible entities. The announcement also explicitly highlights additional eligible applicant categories such as Alaska Native and Native Hawaiian Serving Institutions; Asian American, Native American, and Pacific Islander Serving Institutions (AANAPISIs); Hispanic-serving Institutions; Historically Black Colleges and Universities (HBCUs); Tribally Controlled Colleges and Universities (TCCUs); eligible federal agencies; faith-based or community-based organizations; Indian/Native American tribal governments other than federally recognized ones; regional organizations; U.S. territories or possessions; and non-domestic (non-U.S.) entities (foreign organizations). In effect, NIH designed the eligibility rules to accommodate a wide range of academic, nonprofit, governmental, and industry participants, including institutions serving underrepresented communities and certain international organizations.
Taken together, the FOA is best understood as a targeted push to convert AD genetic signals into experimentally validated biology using human reprogrammed neural cell systems. The expectation is that projects will not only confirm that a variant matters, but also explain how it matters at the level of molecules, pathways, and cell function in human neural cells, thereby illuminating mechanisms that could ultimately be leveraged for diagnostics or therapeutic development.Apply for RFA AG 17 053
- The National Institutes of Health in the health sector is offering a public funding opportunity titled "Human Cell Biology of Genetic Variants in Alzheimer's Disease (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 2016-10-21.
- Applicants must submit their applications by 2017-02-10. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- 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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Frequently Asked Questions (FAQs)
What is the title of this NIH funding opportunity?
The funding opportunity is titled "Human Cell Biology of Genetic Variants in Alzheimer's Disease (R01)."
What is the Funding Opportunity Number (FOA number)?
The FOA number is RFA-AG-17-053.
What CFDA number is associated with this opportunity?
The CFDA number listed is 93.866.
What type of grant mechanism is used?
This opportunity uses the NIH R01 mechanism, which is intended to support substantial, hypothesis-driven research projects with clearly defined aims and rigorous experimental design.
Which agency is offering the grant?
The awarding agency is the National Institutes of Health (NIH).
What is the funding activity category?
The funding activity category is Health.
What is the main purpose of this funding opportunity?
The purpose is to clarify how specific human genetic variants linked to Alzheimer's disease influence brain cell behavior, moving beyond statistical genetic associations to demonstrate causal, functional connections in human neural cells.
What problem is this program trying to address in Alzheimer's genetics research?
Large human genetics studies (such as GWAS and sequencing) can identify genomic regions associated with Alzheimer's risk, but they often do not reveal which gene is affected, the direction of effect, or which cellular pathways are disrupted. This program supports functional follow-up to establish experimentally supported genotype-phenotype relationships.
What does "functional follow-up" mean in the context of this FOA?
It means experimentally testing how Alzheimer's-associated genetic variants alter molecular and cellular phenotypes in relevant human neural cell types, rather than relying only on computational predictions or non-human model systems.
What kinds of genetic variants are in scope for this FOA?
The focus is on human genetic variants suspected of changing Alzheimer's disease risk, including variants identified through genome-wide association studies (GWAS) and genome sequencing efforts.
What is meant by establishing "genotype-phenotype relationships"?
It refers to connecting a specific genetic variant (genotype) to measurable molecular or cellular changes (phenotype) in human neural cells, with evidence supporting a causal relationship.
What model systems are emphasized for the proposed research?
The FOA emphasizes the use of human induced pluripotent stem cells (iPSCs) or other human cell reprogramming methods to generate neural cells for experiments.
Are animal models or immortalized cell lines sufficient for this opportunity?
This FOA emphasizes experiments in human reprogrammed neural systems, based on the rationale that Alzheimer's risk variants may have effects that are difficult to capture in animal models or immortalized cell lines.
What types of human neural cells are expected to be studied?
Projects typically involve differentiating engineered or derived human cell lines into neurons and/or glial cell types such as astrocytes, microglia-like cells, or oligodendrocytes.
Does the FOA require using iPSCs specifically?
The FOA highlights iPSCs as a key requirement of the approach and also notes "other human cell reprogramming methods" to generate neural cells for experiments.
What is the rationale for using human reprogrammed neural cell systems?
The rationale is that human reprogrammed neural systems can better reflect the biology of human brain cells, including gene regulation and disease-relevant pathways, which may be critical for understanding how Alzheimer's risk variants exert their effects.
What kinds of outcomes is NIH looking for?
NIH is looking for experimentally supported links between Alzheimer's genetics and cellular mechanisms, providing causal and functional connections between specific variants and biological changes in human neural cells.
What are examples of molecular phenotypes that could be measured?
Examples include altered gene expression programs, splicing changes, epigenetic states, protein levels, and pathway activation.
What are examples of cellular or biological phenotypes that could be measured?
Examples include changes in neuronal function, synaptic biology, cellular stress responses, inflammatory signaling in glia, protein processing and trafficking, lipid metabolism, and other cell behaviors plausibly connected to Alzheimer's disease etiology.
How does this FOA connect human genetics findings to Alzheimer's disease mechanisms?
It supports research that bridges human genetic discovery (variants linked to Alzheimer's risk) and mechanistic biology by testing variant-driven effects directly in human neural cells and identifying disrupted molecular pathways and cell functions.
How could results from this research be useful for therapy development?
By revealing how specific genetic variants causally alter molecular targets and cellular pathways, the research can sharpen understanding of disease mechanisms and help identify molecular targets that could be relevant for therapeutic development.
What general project characteristics are expected under an R01 for this FOA?
Projects are expected to be substantial and hypothesis-driven, with clearly defined aims, rigorous experimental design, and strong justification for the chosen models and readouts.
When was this opportunity created?
The opportunity record indicates a creation date of October 21, 2016.
What was the original closing date listed for this opportunity?
The listed original closing date was February 10, 2017.
Is the award ceiling provided?
No. The award ceiling is not specified in the provided source data.
Is the expected number of awards provided?
No. The expected number of awards is not specified in the provided source data.
Who is eligible to apply?
Eligibility is broad and includes many types of U.S. organizations and certain non-U.S. entities (foreign organizations) as well.
Are state and local government entities eligible?
Yes. Eligible applicants include state, county, city, township, and special district governments, among other public entities.
Are institutions of higher education eligible?
Yes. Both public/state-controlled institutions of higher education and private institutions of higher education are eligible.
Are nonprofit organizations eligible?
Yes. Nonprofit organizations with or without 501(c)(3) status (other than institutions of higher education) are eligible.
Are for-profit organizations eligible?
Yes. For-profit organizations other than small businesses are eligible, and small businesses are also listed as eligible.
Are tribal organizations eligible?
Yes. Federally recognized Native American tribal governments are eligible, as are other Native American tribal organizations. The announcement also highlights Indian/Native American tribal governments other than federally recognized ones.
Are organizations in U.S. territories or possessions eligible?
Yes. U.S. territories or possessions are explicitly highlighted as eligible.
Are non-U.S. (foreign) organizations eligible?
Yes. The announcement indicates that non-domestic (non-U.S.) entities (foreign organizations) are eligible.
Are minority-serving institutions explicitly included in the eligibility list?
Yes. The FOA explicitly highlights Alaska Native and Native Hawaiian Serving Institutions, AANAPISIs, Hispanic-serving Institutions, Historically Black Colleges and Universities (HBCUs), and Tribally Controlled Colleges and Universities (TCCUs).
Are faith-based or community-based organizations eligible?
Yes. Faith-based or community-based organizations are explicitly highlighted as eligible.
Are eligible federal agencies included?
Yes. Eligible federal agencies are explicitly highlighted as eligible applicants.
Does the FOA specify a preferred approach to linking variants to genes and pathways?
The FOA emphasizes experimentally demonstrating functional, causal connections between Alzheimer's-associated variants and measurable molecular/cellular phenotypes in human neural cells, rather than relying on association signals alone.
What is the overall takeaway of this FOA?
It is a targeted effort to convert Alzheimer's disease genetic signals into experimentally validated biology using human reprogrammed neural cell systems, with the aim of explaining how and why specific variants affect molecules, pathways, and cell function relevant to Alzheimer's disease.
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