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    Mitochondrial-associated Mechanisms of Neuropathological and Immunodeficient Aging in the Context of HIV and SUD (R21 Clinical Trials Not Allowed)

    Study mitochondria, aging, HIV, and substance use to develop therapies for healthier aging in HIV and addiction patients.

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    This grant is no longer accepting proposals

    National Institutes of Health has archived this opportunity.

    Funder: National Institutes of Health

    Due Dates: February 10, 2025 (Letter of Intent & Open Date) | March 10, 2025 (AIDS applications) | March 10, 2026 (AIDS applications)

    Funding Amounts: Up to $275,000 direct costs over 2 years (no more than $200,000 in any single year); 3–6 awards anticipated; total program funding $3M (FY26)

    Summary: Supports exploratory research on mitochondrial mechanisms in aging, HIV infection, and substance use, aiming to inform targeted therapies for people aging with HIV and addiction.

    Key Information: Clinical trials are not allowed; applications must address the intersection of HIV and misused substances (not alcohol alone).


    Description

    This opportunity, offered by the National Institute on Drug Abuse (NIDA) at NIH, seeks to advance foundational research on the interplay between mitochondrial function, aging, HIV infection, and exposure to addictive substances. The goal is to elucidate both protective and pathogenic mechanisms at this nexus, with the expectation that new knowledge will inform the development of targeted therapies and improve health outcomes for people aging with HIV and substance use disorders (SUD).

    Research supported under this program should focus on basic and preclinical studies, including but not limited to:

    • Mitochondrial dynamics, function, metabolomics, and stress responses in the context of HIV and SUD.
    • Mechanisms to alleviate mitochondrial stress and prevent or improve outcomes in people with or at risk for HIV and SUD.
    • Mitochondrial regulation of neural and immune cell activation/senescence, considering HIV status, ART, substance use (including polypharmacy), and age.
    • The role of mitochondrial haplotypes and somatic mutations in neurocognitive impairment and SUD as people with HIV age.
    • Genomic and epigenomic damage from HIV and addictive substances, and their contribution to neuropathogenesis.
    • Computational modeling to identify individuals at risk for pathological aging in the context of HIV and SUD.

    Substances of interest include (but are not limited to): opioids (synthetic and non-synthetic), nicotine, cocaine, methamphetamine, stimulants, psychedelics, xylazine, addictive prescription drugs, cannabinoids, or combinations thereof.

    Note: Applications must address the intersection of HIV and misused substances. Projects focused solely on alcohol as the misused substance are not responsive.


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