The National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA) intend to promote a new initiative by publishing a Funding Opportunity Announcement (FOA) to solicit applications for research on the clinical relevance of the linkage between environmental toxicant exposures and Alzheimer’s Disease and Alzheimer’s Disease Related Dementias (AD/ADRD). There is consensus that environmental toxicants are a risk factor for AD/ADRD, but causality has been largely elusive. While human studies demonstrating an association of AD/ADRD with toxicant exposures are relatively abundant, there is a clear unmet need for more mechanistic research to support or refute the clinical relevance and the biological plausibility of an impact on disease initiation, progression, or modification. This is especially important for understanding the potentially modifiable causes of racial and socioeconomic inequities. The RFA will encourage neuroscientists and environmental health scientists to collaborate and conduct mechanistic AD/ADRD research on the actions of neurotoxicants on the nervous system.
This Notice is being provided to allow potential applicants sufficient time to develop integrated multidisciplinary collaborations and responsive projects.
The FOA is expected to be published in Winter 2022 with an expected application due date in Spring 2022.
This FOA will utilize the R01 activity code.
This Notice encourages neuroscience investigators with expertise and insights into the area of AD/ADRD research to begin to consider applying for this new FOA.
Collaborative investigations combining the expertise of AD/ADRD neuroscientists and environmental health scientists will be strongly encouraged, and these investigators should also begin considering applying for this application.
The RFA will encourage neuroscientists to conduct mechanistic AD/ADRD research on the actions of neurotoxicants on the nervous system. The scope of research includes but is not limited to in silico modeling, in vitro assay development to correlate chemical exposure to AD/ADRD biology, and in vivo studies on the modification of known AD/ADRD targets by neurotoxicants of concern, and conversely, whether known targets for these neurotoxins play a role in the etiology of AD/ADRD. The development and validation of neuropathological, neurophysiological, and neurobehavioral animal models that simulate potential toxicant exposures in humans would be one goal, and when possible, these studies will include comparisons of exposures across the lifespan.
Applications are not being solicited at this time.
Please direct all inquiries to:
David A. Jett