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With a rapidly growing aged U.S. population, maintenance of cognitive function has become increasingly critical for the health, welfare, and well-being of the country's citizens. According to a recent survey conducted by the AARP, virtually all adults age 40+ believe maintaining or improving brain health is important; three-quarters of adults age 40+ are concerned about their brain health declining in the future.  Although chronological age itself remains the strongest predictor of age-related cognitive decline and many forms of dementia, including Alzheimer's disease and Alzheimer's disease-related dementias (AD/ADRD), it has become clear that there are protective factors against these outcomes that are poorly understood. These factors have often been described as imparting resilience or resistance to age-related changes in brain structure or neuropathology, building cognitive and/or brain reserve that would oppose such age-related changes or frank pathology, or augmenting other types of cognitive and brain function that would be beneficial. Some of these protective factors might suggest important intervention strategies.

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.

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.  

This FOA invites Research and Development Center (P30) grant applications in the areas of demography and economics of aging, including relevant interdisciplinary areas rooted in population-based social science research. Areas of focus that are especially encouraged are: a) socioeconomic status (SES) disparities at older ages, including geographic disparities; b) the reasons for poor U.S. performance in health and mortality in international comparisons; c) trends and dynamics in old-age disability; d) cohort trends in obesity and its sequelae; e) family demography including the demography of care and caregiving for chronic disease, disability and Alzheimer's Disease and Alzheimer's-Related Dementias (AD/ADRD); and f) long-term supports and services for the disabled elderly population. Applications that wish to focus exclusively on AD/ADRD should submit to RFA-AG-20-002. Center grant applications must include two mandatory Cores and may choose among three optional Cores. Centers are required to work collaboratively with the Coordinating Center to be funded via RFA-AG-20-003.  

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.

This FOA seeks applications that propose innovative research strategies aimed at increasing the understanding of the changes in cellular architecture that occur during the aging process. Studies on cytoskeleton structure and function, the impact of the cytoskeleton on intracellular organelle interactions, and signaling or regulatory molecules controlling cellular architecture will be considered. There is 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 seeks applications that propose innovative research strategies aimed at increasing the understanding of the changes in cellular architecture that occur during the aging process. Studies on cytoskeleton structure and function, the impact of the cytoskeleton on intracellular organelle interactions, and signaling or regulatory molecules controlling cellular architecture will be considered. There is 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 Funding Opportunity Announcement (FOA) is issued as an initiative of the NIH Blueprint for Neuroscience Research.  The Neuroscience Blueprint is a collaborative framework through which 15 NIH Institutes, Centers and Offices jointly support neuroscience-related research, with the aim of accelerating discoveries and reducing the burden of nervous system disorders (for further information, see http://neuroscienceblueprint.nih.gov/).  The Neuroscience Blueprint is supporting a Lifespan Human Connectome Project (L-HCP) to extend the Human Connectome Project (HCP) (http://www.neuroscienceblueprint.nih.gov/connectome) to map connectivity in the developing, adult, and aging human brain.  The goal of this FOA is to solicit grant applications that propose to extend the experimental protocols developed through the HCP to children in the 0-5 year old age range to investigate the structural and functional changes that occur in the brain during typical development.  Related FOAs solicit applications that apply the HCP protocols to the 5-21 year old age range and to middle age and elderly adults to explore changes that occur during normal aging.  

The goal of this Funding Opportunity Announcement (FOA) is to support research focused on understanding the role of senescence in brain aging and in Alzheimer's disease (AD). This FOA encourages research projects addressing critical knowledge gaps in our understanding of the neurobiology of senescence through cutting-edge techniques, cross-disciplinary collaborations, and/or conceptual innovation, leveraging what is known about senescence in peripheral tissues to learn more about brain aging. Developing a clear understanding of the mechanisms driving aging processes in the brain, including senescence, is essential for combating age-related neurodegenerative diseases.

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.

This Funding Opportunity Announcement (FOA) is issued as an initiative of the NIH Blueprint for Neuroscience Research.  The Neuroscience Blueprint is a collaborative framework through which 15 NIH Institutes, Centers and Offices jointly support neuroscience-related research, with the aim of accelerating discoveries and reducing the burden of nervous system disorders (for further information, see http://neuroscienceblueprint.nih.gov/).  The Neuroscience Blueprint is supporting a Lifespan Human Connectome Project (L-HCP) to extend the Human Connectome Project (HCP) (http://www.neuroscienceblueprint.nih.gov/connectome) to map connectivity in the developing, adult, and aging human brain.  The goal of this FOA is solicit grant applications that propose to extend the experimental protocols developed through the HCP to middle-age and elderly adults to investigate the structural and functional changes that occur in the brain during typical aging.  A companion FOA is soliciting applications that apply the HCP protocols to children and adolescents to explore changes that occur during typical development. 

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.

The purpose of this Funding Opportunity Announcement (FOA) is to encourage basic or clinical research applications that investigate central neural mechanisms of age-related hearing loss in older adults and/or in relevant animal models. This FOA is driven by the need to address a major gap in our understanding of the central pathways and neural networks that are involved in hearing loss, and how these may be altered in the context of the aging brain, as well as how natural aging influences central auditory plasticity.

Recent reports highlight the enormous spatial and temporal diversity of glia, even within the same glial cell type. This within-glial-cell-type heterogeneity evolves during aging, suggesting that subtypes of glia with distinct physiological roles could emerge to influence brain aging processes. The goal of this Funding Opportunity Announcement is to support research addressing critical knowledge gaps in our understanding of how these glial subpopulations could contribute to vulnerability and resilience to brain aging.

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.

The goal of this Funding Opportunity Announcement (FOA) is to support research focused on understanding the role of senescence in brain aging and in Alzheimer's disease (AD). This FOA encourages research projects addressing critical knowledge gaps in our understanding of the neurobiology of senescence through cutting-edge techniques, cross-disciplinary collaborations, and/or conceptual innovation, leveraging what is known about senescence in peripheral tissues to learn more about brain aging. Developing a clear understanding of the mechanisms driving aging processes in the brain, including senescence, is essential for combating age-related neurodegenerative diseases.

This funding opportunity announcement (FOA) invites applications for basic research to better characterize the affective, cognitive, social, and motivational parameters of impaired and intact decision making in both normal aging and Alzheimer's disease (AD). Research is sought that will characterize the extent to which basic behavioral and neural processes involved in decision-making are differentially impacted in normal aging and AD, investigate the influence of social factors on decision-making, and investigate the decision-making factors that render older adults (with or without cognitive impairment) vulnerable to financial exploitation and other forms of mistreatment and abuse. The FOA also invites applications to apply basic research on the processes involved in decision-making to the design of decision-supportive interventions for midlife and older adults with and without AD. Specific opportunities include the development of decision-supportive interventions to leverage cognitive, emotional and motivational strengths of these populations; tools to assess decisional capacity; strategies for simplifying choices and offering better defaults; and the promotion of timely adoption of optimal delegation practices (e.g., power of attorney, living wells, etc.).

This funding opportunity announcement (FOA) invites applications for basic research to better characterize the affective, cognitive, social, and motivational parameters of impaired and intact decision making in both normal aging and Alzheimer's disease (AD). Research is sought that will characterize the extent to which basic behavioral and neural processes involved in decision-making are differentially impacted in normal aging and AD, investigate the influence of social factors on decision-making, and investigate the decision-making factors that render older adults (with or without cognitive impairment) vulnerable to financial exploitation and other forms of mistreatment and abuse. The FOA also invites applications to apply basic research on the processes involved in decision-making to the design of decision-supportive interventions for midlife and older adults with and without AD. Specific opportunities include the development of decision-supportive interventions to leverage cognitive, emotional and motivational strengths of these populations; tools to assess decisional capacity; strategies for simplifying choices and offering better defaults; and the promotion of timely adoption of optimal delegation practices (e.g., power of attorney, living wells, etc.).

This Funding Opportunity Announcement (FOA) invites applications that expand on foundational research demonstrating generally improved emotional function and emotion regulation with aging, to further clarify the trajectories of change in emotion processing and linked neurobiological factors in adults who are aging normally, as well as in individuals with mild cognitive impairment (MCI), Alzheimer's disease, and related dementias (ADRD). The goal is three-fold: to advance understanding of (1) normative maturational shifts in emotional processes, (2) how dysfunction in the integrative neural-behavioral mechanisms of emotional function might manifest in MCI and the early stages of ADRD, and/or (3) how such dysfunction might account for any of the neuropsychiatric symptoms observed in ADRD. Such studies may identify novel targets for interventions or prevention efforts, or provide clues to intervention strategies that might be applied to normalize emotion dysregulation or strengthen emotional resilience at different life stages in normal aging or disease stages in MCI and ADRD.

The purpose of this Funding Opportunity Announcement (FOA) is to encourage basic or clinical research applications that investigate central neural mechanisms of age-related hearing loss in older adults and/or in relevant animal models. This FOA is driven by the need to address a major gap in our understanding of the central pathways and neural networks that are involved in hearing loss and how these may be altered in the context of the aging brain, as well as how natural aging influences central auditory plasticity.

This Funding Opportunity Announcement (FOA) invites applications that expand on foundational research demonstrating generally improved emotional function and emotion regulation with aging, to further clarify the trajectories of change in emotion processing and linked neurobiological factors in adults who are aging normally, as well as in individuals with mild cognitive impairment (MCI), Alzheimer's disease, and related dementias (ADRD). The goal is three-fold: to advance understanding of (1) normative maturational shifts in emotional processes, (2) how dysfunction in the integrative neural-behavioral mechanisms of emotional function might manifest in MCI and the early stages of ADRD, and/or (3) how such dysfunction might account for any of the neuropsychiatric symptoms observed in ADRD. Such studies may identify novel targets for interventions or prevention efforts, or provide clues to intervention strategies that might be applied to normalize emotion dysregulation or strengthen emotional resilience at different life stages in normal aging or disease stages in MCI and ADRD.