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    Mitochondrial-associated Mechanisms of Neuropathological and Immunodeficient Aging in the Context of HIV and SUD (R01 Clinical Trials Not Allowed)

    Research grant explores links between mitochondria, aging, HIV, and substance use to develop therapies for people with HIV and addiction aging effects.

    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) | March 10, 2025 (AIDS applications) | March 10, 2026 (AIDS applications)

    Funding Amounts: ~$3,000,000 total in FY 2026 for 3–6 awards (R01); budgets not limited but must reflect project needs; max project period 5 years.

    Summary: Supports basic and preclinical research on mitochondrial mechanisms of aging in the context of 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 both HIV and substance use (not alcohol alone).


    Description

    This NIH funding opportunity supports research into the protective and pathogenic mechanisms at the intersection of mitochondrial function, aging, HIV infection, and exposure to addictive substances. The goal is to generate foundational knowledge that can be leveraged to develop targeted therapies and improve health outcomes for people aging with HIV and substance use disorders (SUD).

    The program is administered by the National Institute on Drug Abuse (NIDA) and uses the R01 mechanism. Only basic and preclinical research is supported; clinical trials are not allowed.

    Scientific Focus

    Research areas of interest include, but are not limited to:

    • Mechanisms by which mitochondrial dynamics, function, and stress responses contribute to accelerated aging and maintenance of viral reservoirs in people with HIV and SUD.
    • Identification of targetable mechanisms to alleviate mitochondrial stress and improve outcomes in people with or at risk for HIV and SUD.
    • Characterization of mitochondrial regulation in neural and immune cells, considering HIV status, ART, substance use (including polypharmacy), and age.
    • Investigation of mitochondrial haplotypes and somatic mutations in relation to neurocognitive impairment and SUD in aging people with HIV.
    • Genomic and epigenomic damage to mitochondrial and nuclear genomes from HIV and substance use, and their contribution to neuropathogenesis.
    • Development of computational models to identify individuals at risk for pathological aging due to mitochondrial dysfunction in the context of HIV and SUD.

    Note: Applications must focus on the intersection of HIV and misused substances. Projects focused solely on alcohol as the misused substance, or not addressing both HIV and substance use, are not responsive and will not be reviewed.


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