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Since 2017, the National Institute on Aging has sponsored a successful Administrative Supplement program to stimulate the field of Alzheimers disease (AD) and its related dementias (ADRD) (e.g., frontotemporal dementia, Lewy body dementia, Vascular Contributions to Cognitive Impairment and Dementia (VCID), and multiple etiology dementias) (NOT-AG-22-025, NOT-AG-21-018; NOT-AG-20-034; NOT-AG-17-008). This program has especially been effective in bringing researchers into the AD/ADRD research realm. Once more, the participating Institutes and Centers (ICs) are inviting supplement applications to take advantage of this opportunity to support the value of their projects, consistent with the previously peer-reviewed objectives. Therefore, as administrative supplements, the work proposed must be within the scope of the research or training that is already supported in order to be considered for funding. Active awards with project end dates in FY 2025 or later are eligible. The award may not be in a terminal no-cost extension or going into a no-cost extension in FY 2024. Please note that a few ICs limit no-cost extensions in the final non-competing year of an award. For that reason, it is important to contact staff at the IC supporting the award when planning the request.

The purpose of this Funding Opportunity Announcement (FOA) is to support a Chemical Exposure Resource and Coordination Core (ExRC) that will provide infrastructure, management, and research support for studies of Chemicals of Concern (CoC) to the Chemical Countermeasures Research Program (CCRP). This core, established across diverse geographical regions, is intended to support multidisciplinary CCRP investigators, through development of infrastructure and exposure protocols for selected toxicants. The ExRC will provide facility access for using diverse models to characterize pathophysiological mechanisms and evaluating potential medical countermeasures through early-stage development efforts supported by the CCRP.

The ultimate goal is to develop multi-target disease-modifying therapeutics based on an appreciation of the complex interaction of pathways, cells, circuits, systems or pathologies that are present in complex AD/ADRD diagnoses. Such therapeutics could be a single drug or biologic targeting multiple pathways, cell, circuits, systems or pathologies, or could be a combination of therapies. While hundreds of possible targets have been suggested for AD alone, theres a need to better understand how multiple targets might interact in a synergistic way that would allow us to tackle AD/ADRD from multiple fronts in a single person, akin to what has been successful in infectious disease or cancer. This FOA will support applications that test hypotheses of possible beneficial interactions of known targets as well as understanding the mechanisms of interaction in the R61. The R33 would support rigorous validation of the proposed multi-target approach (one drug or biologic targeting multiple pathways; and/or a combination of therapies) to support future multi-target therapy development efforts. Successful grantees will be in position to apply for IGNITE or other similar translational grant mechanisms.

Goal is to have experimental models that can accurately reproduce neuropathological signatures and clinically relevant neurodegenerative, biochemical and behavioral sequelae as those seen in human subjects post-TBI AD/ADRDs. Requirement: Interdisciplinary Team science approach / consortium type of applications. Applications will include multiple sites (3-5 sites) developing and/or testing specific models that will then implement a test of reproducibility across the consortium. Requirement: Must have a clinician with expertise in post-TBI ADRD on the team. Encourage having neuropathologists as consultants on grants. Requirement: Models developed through this FOA will be required to share their model, model details and related standards with the VA-funded interagency preclinical resource center - PRECISE TBI Studies investigating neurodegeneration of white matter and chronic inflammation in post-TBI AD/ADRDs are highly encouraged. Innovative applications reaching beyond the current AD/ADRD models are highly encouraged.

The National Institutes of Health (NIH) intends to support the development of innovative methods for quantitative evaluation of myofascial tissues for pain management involving research participants using a two-phase grant funding mechanism. This effort is part of the NIH HEALSM (Helping to End Addiction Long-term) Initiative to speed the development and implementation of scientific solutions to the national opioid public health crisis. The NIH HEAL Initiative is bolstering research across NIH to (1) improve treatment and prevention of opioid misuse and opioid use disorder and (2) enhance pain management. This notice of funding opportunity (NOFO) seeks research applications to develop quantitative measures of myofascial tissues and assess their abilities to detect changes to myofascial tissues across a variety of pain management interventions. Candidate objective measures may be based on minimally invasive imaging technologies, electrophysiological recordings, integration of multiparametric imaging and electrophysiology approaches, or their integration with other markers (e.g., immune factors, genomic markers, physiological factors) through multiscale modeling or machine learning analysis. The first phase, funded by the R61, will provide funding for up to 3 years to develop quantitative measures that can differentiate abnormal myofascial tissue from healthy tissues using cross-sectional correlations with clinical signs/symptoms. In addition, the R61 phase should include planning activities for the R33 phase. The second phase, funded under the R33, will provide support to assess the abilities of the quantitative measures developed in the R61 phase to measure tissue changes in response to therapies or manipulations that may relieve pain using rigorous, longitudinal clinical study design. The combined R61/R33 should not exceed 5 years. Transition from the R61 to the R33 phase of the award will be administratively reviewed and will be determined based on successful co

"This FOA will solicit R01 applications that propose studies in animal, cell culture, and/or human tissue models to elucidate the mechanisms by which COVID-19 interacts with and/or modulates AD/ADRD-relevant phenotypes. Either the model itself or the experimental readouts will be required to incorporate AD/ADRD risk factors, pathologies, or relevant comorbidities. To this end, proposals can focus on one or more of the following: - Mechanistic studies that address how COVID-19 impacts CNS pathology and cognitive outcomes when AD/ADRD pathology is already present (for example, in a model of AD/ADRD). - Mechanistic studies that address how COVID-19 accelerates AD/ADRD pathology and cognitive deficits in a prodromal model (early phase, pre-symptomatic). - Mechanistic studies that address how COVID-19 predisposes for AD/ADRD and/or interacts with relevant comorbid conditions and risk factors (cellular mechanisms that could potentially increase the risk for future AD/ADRD)."

The goal of this funding opportunity is to develop, establish, implement, and maintain a successful collaborative partnership to advance NIAID priorities, support NIH collaboration on global health, and advance biomedical research internationally. This program will support a partnership between the NIH and the recipient(s) with the commitment and capacity to help extend NIH research-related programs worldwide.

This FOA would support investigations with a minimum of two relevant co-pathologies (e.g., tau, alpha-synuclein, TDP-43, TMEM106B, vascular), with optional risk factors and co-morbidities, to identify cellular and molecular mechanisms of how/why multi-proteinopathy interactions drive worsening neurodegenerative processes and phenotypic outcomes. Studies should examine co-pathology cellular and molecular interactions across brain regions and time in proximate cell population, across various intracellular dynamics and localization, and upstream and downstream from aggregated protein states to determine what events lead to worse phenotypic outcomes.

This FOA would support establishing deeper mechanistic insight and causal relationships between TDP-43 pathology and phenotypic outcomes, as well as mechanistic interactions between TDP-43 and other co-pathologies, such TMEM106B. Additionally, it would include comparisons (including mechanistic, molecular, structural, cellular, genetic, -omic, anatomical, neuropathological, etc.) between TDP-43 proteinopathies, including LATE, with or without AD-NC, and FTD and/or ALS.

This Notice of Funding Opportunity (NOFO) invites applications for a multisite study to comprehensively characterize ADRD relevant pathology related to cognitive impairment and dementia outcomes in persons with a history of traumatic brain injury (TBI). Investigations should elucidate the contribution of key individual (sex, age at time of injury, time since injury, social determinants of health, etc.) and injury characteristics (injury severity and frequency) to describe associations between neuropathological burden and antemortem clinicopathologic symptoms and outline the prevalence of TBI-related ADRD diagnoses, and CTE pathology in the participating brain banks. This NOFO intends to support applications that include retrospective samples, plans to acquire new brain tissue specimens, and methods to assess the antemortem symptomatology and clinical presentation. To further advance research in the area, broad sharing of clinical and neuropathological data will be a critical feature of successful applications, including the development of a digital resource for distribution and sharing of assessed neuropathological tissue.