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Age is the number one risk factor for diagnosis of many age-related lung diseases, including COPD and pulmonary fibrosis. Despite this, little is known regarding the interactions that likely occur between the molecular and cellular mechanisms of disease and the changes in molecules and cells that can be attributed to normal aging. In fact, very little is known about the normal aging process in the lung at the cellular and molecular level. In 2015, the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute on Aging (NIA) co-sponsored a workshop that identified a major knowledge gap in the understanding of normal lung aging in humans, as well as the need to develop a map of molecular changes that occur during normal aging in the lung that can serve as a reference for studies of age-related lung diseases.

Purpose The purpose of this FOA is to support a network to enhance collaborations across NIA's 6 centers programs. These collaborations are intended to leverage NIA's substantial investments by fostering and sustaining the development of novel interdisciplinary efforts in aging research. This opportunity will provide resources to build additional infrastructure and establish specific collaborative activities that could include, but are not limited to, information and data exchange, meetings and conferences, pilot studies, research opportunities for early investigators, visiting scholar programs, dissemination, and other collaborative efforts. The successful awardee will involve all 6 centers programs. Background The National Institute on Aging supports 6 research centers programs: Alzheimer's Disease Centers Claude D. Pepper Older Americans Independence Centers (OAICs) Nathan Shock Centers of Excellence in the Basic Biology of Aging Resource Centers for Minority Aging Research (RCMARs) Edward R. Roybal Centers for Translation Research in the Behavioral and Social Sciences of Aging Centers on the Demography and Economics of Aging These programs, comprised of over 80 individual centers across the US, are highly productive hubs of research activity that are advancing the science of aging in their individual areas of focus. As advances in one area have the potential to address obstacles to progress in another area, numerous opportunities exist for collaborations across different centers programs. However, these opportunities have been realized to only a limited degree to date.

The purpose of this FOA is to support the development of a Clinician-Scientists Transdisciplinary Aging Research (Clin-STAR) Coordinating Center that will organize activities and provide research resources for clinician-investigators across the United States who are focusing their careers on aging research. This FOA is intended to build upon the substantial investments made by NIA through the GEMSSTAR program and related career development efforts by supporting expanded activities to reach a broader community of clinician-investigators. The specific goals of this initiative are to convey scientific and research knowledge on aging research; foster networking and collaboration between clinician-scientist leaders in aging research and clinician-investigators across specialties who wish to focus on aging research; provide mentoring and career development support for emerging clinician-scientists committed to pursuing aging research in their clinical specialty or discipline; and advance transdisciplinary research projects in aging. Ultimately, the Clin-STAR Coordinating Center is intended to provide a multi-faceted national research platform leading to improved patient-centered care for older adults across specialties and disciplines.

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/cross talk 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 emergent field of geroscience seeks to relate the biology of aging to the development of chronic diseases and the onset of degenerative conditions which are prevalent in the older segment of human populations. It is generally accepted that age is the major risk factor for most chronic diseases and degenerative conditions in adults. Thus, a critical question in geroscience is to identify components in the biology of aging that are the underlying risk for multiple chronic diseases and degenerative conditions. Therefore, this FOA will support planning grants to circumscribe the scope of this question and suggest ways to answer it experimentally. The focus will be on epigenetics underlying aging as a risk factor for age-related diseases and degenerative conditions in humans. Mortality and age-related mortality are outside the scope of this FOA. Studies using model organisms are outside the scope of this FOA.

This Funding Opportunity Announcement (FOA) invites applications proposing research on the specific role of aging biology in the development, etiology and treatment of Alzheimer's disease. Aging is by far the main risk factor for most chronic diseases, a fact recognized by the field of geroscience. Recent advances in the fields of basic aging biology and geroscience now allow researchers to address mechanistically the role of aging in Alzheimer's disease. Applications that make use of geroscience principles and test the role of different hallmarks of aging biology are specifically appropriate, while those focused solely on aging biology, or solely on Alzheimer's disease will be deemed nonresponsive to the FOA.

This Funding Opportunity Announcement (FOA) invites applications proposing research on the specific role of aging biology in the development, etiology and treatment of Alzheimer's disease. Aging is by far the main risk factor for most chronic diseases, a fact recognized by the field of geroscience. Recent advances in the fields of basic aging biology and geroscience now allow researchers to address mechanistically the role of aging in Alzheimer's disease. Applications that make use of geroscience principles and test the role of different hallmarks of aging biology are specifically appropriate, while those focused solely on aging biology, or solely on Alzheimer's disease will be deemed nonresponsive to the FOA.

The National Institute on Aging (NIA) solicits research projects that would advance our understanding of how protein homeostasis (proteostasis) in peripheral tissues affects brain aging, leading to the development of Alzheimers Disease (AD). Much research on AD has focused on the accumulation of aberrant protein aggregates in the brain, and in particular amyloid and Tau. Formation of aggregates due to mutations encoded in the APP gene or due to hyperphosphorylation, respectively, have been linked to familial AD. The etiology of the more common, sporadic form of AD, is less certain, although aging is considered a major risk for development of the disease. It is known that proteostasis is less efficiently maintained in all tissues with aging, and this may indicate a link between proteostasis in the periphery and the appearance of aging-related diseases and conditions, including the decline in cognitive function, as well as dementia and AD. Therefore, testing for a role of aging-related loss of peripheral proteostasis in the development of AD is the focus of this FOA.

This Funding Opportunity Announcement (FOA) encourages applications to develop valid markers to assess the activity of fundamental aging mechanisms in humans that may influence the risk and progression of multiple aging conditions. Projects are encouraged that focus on selected mechanism(s) that may regulate aging changes, assess multiple possible markers for these mechanisms, test methods to improve their measurement properties, characterize their variability among individuals of differing ages and within the same age cohort, and assess their relationships in humans to in vivo functions influenced by the mechanism(s) under study. It is strongly encouraged that each project includes an interdisciplinary research team with expertise, as needed, in the biology of their selected mechanism(s), biomedical aging research, clinical pathology including laboratory assays, imaging methods, human cohort studies, tissue banking, biorepository resources, and statistics. Though the principal focus of the initiative is on development of markers in humans, studies in laboratory animals may also be conducted when necessary for the development of human markers, and potential development of parallel laboratory animal markers of a given mechanism.

The participating NIH Institutes and Centers invite applications to address both the origins and the effects of low level chronic inflammation in the onset and progression of age-related diseases and conditions. Chronic inflammation, as defined by elevated levels of both local and systemic cytokines and other pro-inflammatory factors, is a hallmark of aging in virtually all higher animals including humans and is recognized as a major risk factor for developing age-associated diseases. The spectra of phenotypes capable of generating low-level chronic inflammation and their defining mediators are not clear. Further, a clear understanding of how chronic inflammation compromises the integrity of cells or tissues leading to disease progression is lacking. The role of dietary supplements and/or nutritional status in chronic inflammation in age-related disease is also poorly studied. Thus, there is a critical need to establish the knowledge base that will allow a better understanding of the complex interplay between inflammation and age-related diseases. Applications submitted to this FOA should aim to clarify the molecular and cellular basis for the increase in circulating inflammatory factors with aging, and/or shed light on the cause-effect relationship between inflammation and disease, using pre-clinical (animal or cellular based) models.

This Funding Opportunity Announcement (FOA) invites applications proposing research on the specific role of aging biology in the development, etiology and treatment of Alzheimer's disease. Aging is by far the main risk factor for most chronic diseases, a fact recognized by the field of geroscience. Recent advances in the fields of basic aging biology and geroscience now allow researchers to address mechanistically the role of aging in Alzheimers disease. Applications that make use of geroscience principles and test the role of different hallmarks of aging biology are specifically appropriate, while those focused solely on aging biology, or solely on Alzheimers disease will be deemed unresponsive to the FOA.

This Funding Opportunity Announcement (FOA) invites applications proposing research on the specific role of aging biology in the development, etiology and treatment of Alzheimer's disease. Aging is by far the main risk factor for most chronic diseases, a fact recognized by the field of geroscience. Recent advances in the fields of basic aging biology and geroscience now allow researchers to address mechanistically the role of aging in Alzheimers disease. Applications that make use of geroscience principles and test the role of different hallmarks of aging biology are specifically appropriate, while those focused solely on aging biology, or solely on Alzheimers disease will be deemed unresponsive to the FOA.

This FOA invites applications on novel studies of the molecular mechanisms underlying metformin's effects on aging and longevity. The goal of this FOA is to support applications that will lead to an in-depth understanding of the molecular mechanisms that determine the effects of metformin, either beneficial or detrimental, in relation to aging and longevity. Research supported by this FOA should lead to new insights on and better understanding of metformin's effects on aging and aging-related diseases.

The involvement of small businesses in translational aging research could substantially hasten the pace at which scientific advances are transformed into commercial products to improve or maintain the health and functional independence of older adults. Therefore, this funding opportunity announcement (FOA) is intended to encourage a greater involvement by small businesses through the SBIR mechanism in transforming scientific advances in aging research into novel devices, products, health care practices and programs that will benefit the lives of older adults. For the purposes of this FOA, T1 translational research on aging is defined as the application of basic and clinical biomedical or basic behavioral and social research findings towards the development of new strategies for prevention and treatment of age-related pathologies. T1 translational research approaches could include the development of new research tools or improving existing technologies to diagnose, prevent or treat age-related conditions, functional decline and disability.

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 goal of this FOA is to advance research on the underlying basis for the transfer (or transposition) of aging phenotypes observed between young and old rodents and discovered through heterochronic parabiosis. Examples of transposed phenotypes include reversal of cardiac hypertrophy, partial restoration of cognitive function, improved vascularization, and repair of skeletal muscle after cryo-injury (anti-geronic transposition), or as accelerated loss of cognitive function and neurogenesis (pro-geronic transposition). Other transposed phenotypes, as revealed solely through heterochronic parabiosis, may also be reported in the literature. There are also reports of candidate factors found in circulation that might be causally related to the transposition of these aging phenotypes; these are termed "circulating geronic factors" for purposes of this FOA. To date, these are proteins and peptides that pass between the young and old mice joined by parabiosis, due to anastomosis of their circulatory systems. Based on these novel findings and this novel experimental paradigm, the specific objective of this FOA is to test whether these candidate geronic factors are necessary for the transposition of aging phenotypes. The focus is on phenotypes transposed in heterochronic parabiosis and the candidate factors which are present and functional at physiological concentrations in circulation.

The goal of this FOA is to advance research on the underlying basis for the transfer (or transposition) of aging phenotypes observed between young and old rodents and discovered through heterochronic parabiosis. Examples of transposed phenotypes include reversal of cardiac hypertrophy, partial restoration of cognitive function, improved vascularization, and repair of skeletal muscle after cryo-injury (anti-geronic transposition), or as accelerated loss of cognitive function and neurogenesis (pro-geronic transposition). Other transposed phenotypes, as revealed solely through heterochronic parabiosis, may also be reported in the literature. There are also reports of candidate factors found in circulation that might be causally related to the transposition of these aging phenotypes; these are termed "circulating geronic factors" for purposes of this FOA. To date, these are proteins and peptides that pass between the young and old mice joined by parabiosis, due to anastomosis of their circulatory systems. Based on these novel findings and this novel experimental paradigm, the specific objective of this FOA is to test whether these candidate geronic factors are necessary for the transposition of aging phenotypes. The focus is on phenotypes transposed in heterochronic parabiosis and the candidate factors which are present and functional at physiological concentrations in circulation.

The overall goal of this funding announcement is to solicit applications to investigate the central neural control of mobility in older adults without overt neurological diseases using innovative and cutting-edge methods that are emerging in neuroscience, geriatrics and mobility-related fields in aging research communities. This announcement also seeks information on the degree of plasticity in the aging brain and how this may be harnessed to maintain or improve mobility. Applicants are highly encouraged to adapt a multidisciplinary and collaborative approach that includes basic, clinical, and translational scientists. Mobility impairments are common in aging and are associated with a host of adverse events including disability and mortality. Identifying novel modifiable predictors of mobility decline will lead to mechanistic insights and the development of novel therapeutic interventions to enhance mobility as a person ages.

This FOA invites applications on novel studies of the molecular mechanisms underlying metformins effects on aging and longevity. The goal of this FOA is to support applications that will lead to an in-depth understanding of the molecular mechanisms that determine the effects of metformin, either beneficial or detrimental, in relation to aging and longevity. Research supported by this FOA should lead to new insights and better understanding of metformins effects on aging and aging-related diseases.

The purpose of this FOA is to stimulate the development of innovative research strategies aimed at increasing the understanding of the molecular and cellular changes in the cytoskeleton that occur during the aging process.  Applications considering the effect of age on factors such as cytoskeleton structure and function, the impact of the cytoskeleton on intracellular organelle interactions, and signaling or regulatory molecules controlling cellular architecture are encouraged.  There is also interest in studying the role of the cytoskeleton in nuclear-cytoplasmic communications, and in spatio-temporal relationships during the aging process and in age-related diseases.

This FOA is soliciting research projects that would advance biomedical research on the role of peripheral proteostasis on brain structure and function during aging and in Alzheimer's disease, facilitating the identification of molecular and cellular markers of normal brain aging and brain aging during pathological conditions.