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This Small Research Grant Program supports important and innovative research in areas in which more scientific investigation is needed to improve the prevention, diagnosis, treatment and care for Alzheimer's disease and related dementias. The program seeks to stimulate the next generation of researchers in the United States to pursue research and academic careers in neurosciences, Alzheimer's disease and healthy brain aging.

This Funding Opportunity Announcement (FOA) invites applications for P30 Alzheimer's Disease Research Centers. NIA-designated Alzheimer's Disease Research Centers (ADRCs) serve as major sources of discovery into the nature of Alzheimer's disease (AD) and related dementias and into the development of more effective approaches to prevention, diagnosis, care, and therapy. They contribute significantly to the development of shared resources that support dementia-relevant research, and they collaborate and coordinate their research efforts with other NIH-funded programs and investigators.

This funding opportunity announcement (FOA) supports the development of PET radioligands that identify proteinopathies or pathological processes associated with the human biology of Alzheimer's disease related dementias (ADRDs). Activities supported under this FOA include, but are not limited to the in vitro screening of existing ligands against human ADRD brain tissue, medicinal chemistry support for development of new compounds and improvement of existing ligand specificity and selectivity, initial screening of ligands in appropriate animal models, and radioligand formulation and first-in-human testing. The Center without Walls should encompass research that will move promising ligands through in vitro and in vivo optimization to first-in-human studies. Applications must include an administrative core, a medicinal chemistry core, a clinical core, a scientific governance structure, and a minimum of two research projects with milestone plans that address workflows for screening of existing and newly derived ligands against human ADRD tissue and appropriate animal models. Synergy must be evident among Center research projects and cores, such that successful completion of the aims could not be accomplished without the Center structure.

The purpose of the FOA is to support the structural characterization of protein species associated with Alzheimer's Disease Related Dementias (ADRDs) through the utilization of cryo-electron microscopy (cryo-EM) and cryo-electron tomography (cryo-ET) of proteins expressed in human tissue and cell sources. Studies in response to this RFA should also include the development of research tools and resources to further characterize/validate the protein species.

The purpose of this Funding Opportunity Announcement (FOA) is to invite applications proposing research on current topics in Alzheimer's disease and its related dementias. Further information on the high priority topics of interest will be announced through a series of notices published in late January and early February of 2018.

This Funding Opportunity Announcement (FOA) enables data-driven drug repositioning and combination therapy for Alzheimer's disease and Alzheimer's disease-related dementias (AD/ADRD) by developing computational methods and data resources and/or integrating computational approaches with proof-of-concept efficacy studies in cell-based models, animal models, and/or humans.

Translational Bioinformatics Approaches to Advance Drug Repositioning and Combination Therapy Development for Alzheimer's Disease (R01 Clinical Trial Optional)

The National Institute on Aging is seeking applications on systems biology approaches using non-mammalian laboratory animal models to increase our understanding of the basic biology underpinning neurodegeneration. It is expected that research supported under this FOA will provide new insights into molecular networks that might be involved in causing, amplifying or protecting against neurodegeneration, and that, in turn, might ultimately contribute to Alzheimer's disease or related dementias. Importantly, a major goal of this FOA is to use interaction and regulatory networks produced and analyzed using systems biology to gain these new insights. Because this FOA is directed toward discovery, currently employed genetically modified laboratory animals used to study AD are not required, although they may be used. Because this FOA requires systems biology approaches, data used to build interaction or regulatory networks may also come from humans or other mammals in which AD, related dementias, or aging-related cognitive decline have been observed. This FOA will only support studies using non-mammalian laboratory animal models; studies involving humans or experiments with mammals will not be allowed under this FOA.

The National Institute on Aging is seeking applications on systems biology approaches using non-mammalian laboratory animal models to increase our understanding of the basic biology underpinning neurodegeneration. It is expected that research supported under this FOA will provide new insights into molecular networks that might be involved in causing, amplifying or protecting against neurodegeneration, and that, in turn, might ultimately contribute to Alzheimer's disease or related dementias. Importantly, a major goal of this FOA is to use interaction and regulatory networks produced and analyzed using systems biology to gain these new insights. Because this FOA is directed toward discovery, currently employed genetically modified laboratory animals used to study AD are not required, although they may be used. Because this FOA requires systems biology approaches, data used to build interaction or regulatory networks may also come from humans or other mammals in which AD, related dementias, or aging-related cognitive decline have been observed. This FOA will only support studies using non-mammalian laboratory animal models; studies involving humans or experiments with mammals will not be allowed under this FOA.

Multimorbidity, having two or more chronic conditions, is a complex challenge for doctors. This challenge becomes even more complex when treating patients with Alzheimer's disease and related dementia (ADRD), as the clinical presentation and prolonged course of ADRD influence the diagnosis and treatment of comorbid illness. Compared to patients with other long-term disorders, those with dementia may have extreme multimorbidity, averaging four additional chronic medical disorders. The most common chronic comorbid conditions for ADRD patients are hypertension and diabetes, but other significant comorbidities include, but are not limited to, heart disease, heart failure, obstructive lung disease, and incontinence, as well as acute conditions like infectious diseases and hip fracture.

To date, the pursuit of disease-modifying therapy development for Alzheimer's disease (AD) has been primarily informed by the study of diseased individuals, often by comparing genomic and other molecular, cellular and physiologic features in AD cases and controls. This has proven extremely challenging given the disease's heterogeneity and its multifactorial etiology. There is a growing appreciation that the development of effective treatment and prevention for complex diseases such as AD can benefit from gaining a much deeper understanding of what it means to be well and which genomic, epigenomic, environmental, social, and behavioral factors promote wellness and protection against disease.

This FOA is aimed at molecular, cellular, genetic, epigenetic, and systems biology approaches to advance basic and clinical research on the causes and consequences of sleep deficiency and circadian clock dysfunction in Alzheimer's disease, and the roles of sleep and the circadian clock as modifiers of the progression of neurodegeneration.

This FOA invites applications on descriptive, basic and translational studies of APOE2 to delineate the functional effects of ApoE2 on healthy aging of the brain and other tissues. The primary focus is on the "ApoE2-Aging-AD" relationship and the mechanistic effects of the protective variant on aging and potential interaction/crosstalk between tissues in the aging process and AD. These studies are expected to generate new mechanistic insights that involve brain and/or other organs and assist in the identification of potential prognostic and diagnostic markers and therapeutic targets for AD and other age-related cognitive disorders. Eventually, the findings from these studies could lead to translational research opportunities not only to prevent or delay the onset of AD, but also to protect against multiple age-related conditions.

The purpose of this Funding Opportunity Announcement (FOA) is to encourage applications that propose either basic, clinical, or a combination of basic and clinical studies to investigate how functional changes in the sensory and/or motor systems impact the development and progression of Alzheimer's disease. Studies may include older adults and/or animal models and may employ a variety of approaches, including cellular, molecular, imaging, physiological and genetic, to address this need. For clinical studies, leveraging of existing longitudinal cohorts already collecting sensory and motor assessments is highly encouraged.

This funding opportunity (FOA) encourages small business technology transfer STTR research and development of commercial pharmaceutical interventions to extend lifespan and/or healthspan, to prevent, treat, and/or slow the progression of symptoms associated with Alzheimer's disease (AD) or Alzheimer's disease related dementia (ADRD) in human cells and/or tissue, in-vitro models, and/or non-human animals.

This funding opportunity announcement (FOA) invites research to develop, characterize, and validate new, unconventional, or innovative non-rodent mammalian models of late-onset (sporadic) Alzheimer's Disease (AD). These new models are expected torecapitulate molecular, cellular, neuropathological, behavioral, and/or cognitive hallmarks and aspects of late-onset AD.Research supported under this FOA is expected to provide new investigativetools to identify the gaps in current knowledge related to molecular mechanisms of late-onset AD and identify potential therapeutic targets.