Opportunity Information: Apply for PA 14 139
Apply for PA 14 139
- The National Institutes of Health in the health sector is offering a public funding opportunity titled "Neuroimmune Mechanisms of Alcohol Related Disorders (R01)" and is now available to receive applicants.
- Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.273 Alcohol Research Programs.
- This funding opportunity was created on Mar 3, 2014 and posted on Mar 3, 2014.
- Applicants must submit their applications by May 7, 2017. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- Eligible applicants include: Public and State controlled institutions of higher education Special district governments City or township governments Independent school districts Public housing authorities/Indian housing authorities Nonprofits that do not have a 501(c)(3) status with the IRS, other than institutions of higher education County governments Native American tribal governments (Federally recognized) Others (see text field entitled Additional Information on Eligibility for clarification) Native American tribal organizations (other than Federally recognized tribal governments) For profit organizations other than small businesses Small businesses Nonprofits having a 501(c)(3) status with the IRS, other than institutions of higher education Private institutions of higher education State governments.
- Other Eligible Applicants include the following Alaska Native and Native Hawaiian Serving Institutions Asian American Native American Pacific Islander Serving Institutions (AANAPISISs) Eligible Agencies of the Federal Government Faith based or Community based Organizations Hispanic serving Institutions Historically Black Colleges and Universities (HBCUs) Indian/Native American Tribal Governments (Other than Federally Recognized) Non domestic (non U.S.) Entities (Foreign Organizations) Regional Organizations Tribally Controlled Colleges and Universities (TCCUs) U.S. Territory or Possession Non domestic (non U.S.) Entities (Foreign Institutions) are eligible to apply. Non domestic (non U.S.) components of U.S. Organizations are eligible to apply. Foreign components, as defined in the NIH Grants Policy Statement, are allowed.
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Opportunity Summary:
The Neuroimmune Mechanisms of Alcohol Related Disorders (R01) funding opportunity (PA 14-139) is a National Institutes of Health (NIH) discretionary grant announcement that supports investigator-initiated Research Project Grant (R01) applications focused on how alcohol exposure affects neuroimmune signaling in the brain and how those immune-related changes translate into the functional and behavioral features of alcohol use disorders. The central motivation behind the program is that a growing body of evidence from animal models and analyses of post mortem brain tissue from individuals with alcohol dependence indicates alcohol can meaningfully alter the brain's neuroimmune system. Even with that evidence in hand, the field still lacks clear, causal explanations for how disrupted or rewired neuroimmune signaling contributes to the brain changes that sustain dependence, relapse vulnerability, cognitive and emotional dysregulation, and other alcohol-related behavioral outcomes. This FOA is meant to close that gap by encouraging mechanistic studies that connect neuroimmune alterations to neuroadaptations in circuits, synapses, developmentally relevant processes, and neuroendocrine regulation.
A key scientific theme emphasized in the announcement is the expanding understanding that neuroimmune molecules are not limited to classical immune roles or to immune cells alone. Many of these molecules are expressed in both neurons and glial cells, and they can act as neuromodulators that influence synaptic function, neurodevelopment, and neuroendocrine activity. In practical terms, that means investigators are encouraged to treat neuroimmune factors as active components of brain signaling and plasticity, not simply as byproducts of inflammation. Because these same molecules also sit at the center of neuroinflammatory processes, the FOA frames neuroimmune biology as a unifying lens for understanding how alcohol can drive lasting brain adaptations and corresponding behavioral phenotypes. The research supported under this opportunity is expected to deliver fundamental insight into the neuroimmune mechanisms that underlie alcohol-induced changes in brain function and behavior, and to help clarify when immune-like signaling is adaptive, maladaptive, or both across different stages of alcohol exposure and dependence.
From an administrative and eligibility standpoint, this opportunity uses the R01 funding instrument, falls under the health funding activity category, and is listed under CFDA 93.273 (Alcohol Research Programs). There is no cost sharing or matching requirement. The announcement was posted March 3, 2014, with an original and current closing date of May 7, 2017, and an archive date of June 7, 2017, meaning it is no longer active but remains relevant as a reference point for NIH priorities and for understanding the kinds of projects NIH has historically solicited in this space. A wide range of applicant organizations were eligible, including public and private institutions of higher education, nonprofits (including those with and without 501(c)(3) status), for-profit organizations (including small businesses and other for-profits), and multiple levels of government entities (state, county, city/township, special districts), along with tribal governments and tribal organizations. The FOA also explicitly included eligibility for a variety of mission-specific institutions (for example, HBCUs, Hispanic-serving institutions, tribally controlled colleges and universities, Alaska Native and Native Hawaiian-serving institutions, and AANAPISI institutions), faith-based and community-based organizations, and federal agencies. Importantly, foreign organizations and foreign institutions were eligible to apply, and foreign components of U.S. organizations were allowed consistent with NIH policy.
In summary, PA 14-139 was designed to push the field beyond documenting that alcohol influences inflammatory markers or immune-related pathways and toward demonstrating mechanisms: identifying which neuroimmune signals change with alcohol exposure, where in the brain those changes occur (cell types and circuits), how those signals reshape synaptic and neuroendocrine function, and how those biological effects map onto dependence-relevant behaviors. The overarching goal is to build a more precise framework for understanding alcohol use disorders through neuroimmune biology, creating a foundation that can later inform prevention strategies, biomarkers, and therapeutic approaches targeting neuroimmune pathways.
Frequently Asked Questions (FAQs): Neuroimmune Mechanisms of Alcohol Related Disorders (R01) (PA 14-139)
What is the Neuroimmune Mechanisms of Alcohol Related Disorders (R01) funding opportunity?
PA 14-139 is a National Institutes of Health (NIH) discretionary grant announcement that supported investigator-initiated Research Project Grant (R01) applications focused on neuroimmune signaling in the brain in the context of alcohol exposure and alcohol use disorders.
What type of NIH award mechanism did this opportunity use?
This opportunity used the R01 funding instrument (Research Project Grant), which supports investigator-initiated research projects.
What scientific problem was this FOA trying to address?
The FOA targeted a key gap in the field: while evidence from animal models and post mortem brain tissue analyses suggests alcohol can alter the brain neuroimmune system, there has been a lack of clear causal, mechanistic explanations for how disrupted or rewired neuroimmune signaling drives the brain and behavioral changes linked to alcohol dependence and alcohol use disorders.
What kinds of research questions were emphasized?
The announcement emphasized mechanistic studies that connect alcohol-related neuroimmune alterations to neuroadaptations in brain circuits and synapses, developmentally relevant processes, neuroendocrine regulation, and dependence-relevant behavioral outcomes.
What does the FOA mean by "neuroimmune signaling" in this context?
In this program’s framing, neuroimmune signaling refers to immune-related molecules and pathways in the brain that can influence brain function. The FOA emphasized that these molecules are not limited to classical immune roles or immune cells; they may be expressed in neurons and glial cells and can act as neuromodulators affecting synaptic function, neurodevelopment, and neuroendocrine activity.
Why did this FOA emphasize neuroimmune molecules as "active components" rather than simply inflammation markers?
The FOA highlighted that neuroimmune molecules can directly participate in brain signaling and plasticity, not merely appear as secondary byproducts of inflammation. At the same time, these molecules can also be central to neuroinflammatory processes, making neuroimmune biology a unifying lens for understanding how alcohol can drive lasting brain and behavioral adaptations.
What evidence motivated this funding opportunity?
The central motivation was a growing body of evidence from animal models and analyses of post mortem brain tissue from individuals with alcohol dependence indicating that alcohol can meaningfully alter the brain’s neuroimmune system.
What behavioral or clinical features of alcohol use disorders were specifically mentioned as relevant outcomes?
The FOA pointed to dependence, relapse vulnerability, cognitive dysregulation, emotional dysregulation, and other alcohol-related behavioral outcomes as key features that mechanistic neuroimmune research should help explain.
What kinds of biological targets or systems were highlighted as important to connect to neuroimmune alterations?
The announcement specifically called for connecting neuroimmune alterations to neuroadaptations in circuits and synapses, developmentally relevant processes, and neuroendocrine regulation.
What was the expected impact of research supported by this opportunity?
Supported research was expected to deliver fundamental insight into neuroimmune mechanisms underlying alcohol-induced changes in brain function and behavior, and to clarify when immune-like signaling is adaptive, maladaptive, or both across different stages of alcohol exposure and dependence.
Did the FOA focus only on documenting changes in inflammatory markers?
No. A core goal was to push the field beyond documenting that alcohol influences inflammatory markers or immune-related pathways, and toward demonstrating mechanisms: which neuroimmune signals change with alcohol exposure, where those changes occur in the brain (including cell types and circuits), how they reshape synaptic and neuroendocrine function, and how those biological effects map to dependence-relevant behaviors.
Where in the brain did the FOA encourage investigators to localize neuroimmune changes?
The FOA encouraged studies that identify where changes occur in the brain, including which cell types are involved and which circuits are affected.
What stages of alcohol exposure or dependence were considered important?
The FOA explicitly noted the importance of understanding neuroimmune signaling across different stages of alcohol exposure and dependence, including distinguishing adaptive versus maladaptive immune-like signaling (or cases where it may be both).
What funding activity category did this opportunity fall under?
This opportunity was listed under the health funding activity category.
What is the CFDA number associated with this opportunity?
The opportunity was listed under CFDA 93.273 (Alcohol Research Programs).
Was cost sharing or matching required?
No. The opportunity stated there was no cost sharing or matching requirement.
When was the announcement posted?
The announcement was posted on March 3, 2014.
What were the closing and archive dates for this FOA?
The original and current closing date was May 7, 2017. The archive date was June 7, 2017.
Is this funding opportunity still active?
No. Based on the closing and archive dates provided, it is no longer active. It remains relevant as a reference point for NIH priorities and the types of projects NIH has historically solicited in this research area.
Who was eligible to apply?
A wide range of organizations were eligible, including public and private institutions of higher education; nonprofits (with or without 501(c)(3) status); for-profit organizations (including small businesses and other for-profits); and multiple levels of government entities (state, county, city/township, and special districts), as well as tribal governments and tribal organizations.
Were mission-specific and minority-serving institutions included in eligibility?
Yes. The FOA explicitly included eligibility for a variety of mission-specific institutions, including HBCUs, Hispanic-serving institutions, tribally controlled colleges and universities, Alaska Native and Native Hawaiian-serving institutions, and AANAPISI institutions.
Could faith-based or community-based organizations apply?
Yes. The FOA explicitly included faith-based and community-based organizations among eligible applicants.
Were federal agencies eligible to apply?
Yes. Federal agencies were listed as eligible applicants.
Could foreign organizations or institutions apply?
Yes. Foreign organizations and foreign institutions were eligible to apply.
Were foreign components of U.S. organizations allowed?
Yes. Foreign components of U.S. organizations were allowed, consistent with NIH policy.
What overarching long-term goal did the FOA articulate?
The FOA’s overarching goal was to build a more precise framework for understanding alcohol use disorders through neuroimmune biology, creating a foundation that can later inform prevention strategies, biomarkers, and therapeutic approaches targeting neuroimmune pathways.
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