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Robert Vassar - US grants
Affiliations: | Northwestern University, Evanston, IL |
Area:
Alzheimer'sWebsite:
http://www.feinberg.northwestern.edu/~igp/facindex/VassarR.htmlWe are testing a new system for linking grants to scientists.
The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
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High-probability grants
According to our matching algorithm, Robert Vassar is the likely recipient of the following grants.Years | Recipients | Code | Title / Keywords | Matching score |
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2003 — 2019 | Vassar, Robert J | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Bace1 as a Therapeutic Target For Alzheimer's Disease @ Northwestern University Lowering Abeta levels and reducing amyloid deposition in the brain may be efficacious for Alzheimer's disease (AD). Abeta is the main component of amyloid plaques, and Abeta(42) correlates with AD. The beta-secretase, BACE1, is the enzyme that initiates Abeta generation and therefore it (and gamma-secretase) is a prime drug target for AD. The p3 peptide (Abeta17-40/42), the product alpha of gamma-secretase cleavage, is a major component of diffuse amyloid plaques that form early in AD. p3 is assumed to be non-amyloidogenic, however this has not been rigorously tested in vivo. We will study this question using BACE1 deficient mice, which have high levels of p3 and lack Abeta in the brain. In principle, the combined inhibition of both BACE1 and 7-secretase may more effectively reduce Abeta levels and amyloid deposition than inhibition of either enzyme alone. We will test this hypothesis by analyzing mice with compound BACE1 and presenilin heterozygous null mutations. Finally, the value of BACE1 as a drug target depends on whether BACE1 inhibition is free of toxic side effects, which in turn depends on the physiological functions of BACE1. To elucidate BACE1 functions, we will determine pathways and substrates of BACE1 using genomic and proteomic approaches. Our overall hypothesis is that BACE1 is a valid drug target for AD. The long-term goal of this project is to provide evidence that BACE1 inhibition is likely to be beneficial and have low toxicity for the treatment of AD. The Specific Aims are the following: 1. Determine whether p3 is amyloidogenic in vivo; 2. Determine whether combined genetic reduction of BACE1 and presenilin is more effective for decreasing Abeta production and amyloid deposition than reduction of either enzyme alone; 3. Identify BACE1 physiological functions and substrates using genomic and proteomic strategies. We will use transgenic and knockout mice and cultured primary neurons as model systems. Analytical approaches will include molecular (Northern, RTPCR, Western, immunoprecipitation, ELISA, gene microarray, 2D-PAGE, protein fingerprinting) and cellular (immunohistochemistry/light microscopy, immunofluoescence/confocal microscopy) techniques. These Aims will test our overall hypothesis that BACE1 is a valid drug target, and we expect our results will strengthen the conceptual foundation for the development of BACE1 and gamma-secretase inhibitors for AD. |
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2007 | Vassar, Robert J | P01Activity Code Description: For the support of a broadly based, multidisciplinary, often long-term research program which has a specific major objective or a basic theme. A program project generally involves the organized efforts of relatively large groups, members of which are conducting research projects designed to elucidate the various aspects or components of this objective. Each research project is usually under the leadership of an established investigator. The grant can provide support for certain basic resources used by these groups in the program, including clinical components, the sharing of which facilitates the total research effort. A program project is directed toward a range of problems having a central research focus, in contrast to the usually narrower thrust of the traditional research project. Each project supported through this mechanism should contribute or be directly related to the common theme of the total research effort. These scientifically meritorious projects should demonstrate an essential element of unity and interdependence, i.e., a system of research activities and projects directed toward a well-defined research program goal. |
Astrocytic Bace1 Expression and Beta-Amyloid Peptide Generation @ Northwestern University Amyloid plaques are a major pathological hallmark of Alzheimer's disease (AD). The beta-amyloid peptide (Abeta) is the main component of amyloid plaques, and evidence suggests that Abeta is central to AD pathogenesis. Abeta is generated from the amyloid precursor protein (APP) via sequential cleavage by two proteases, the beta- and gamma-secretases. The beta- secretase, a novel aspartic protease termed BACE1, was initially cloned and characterized in our group. BACE1 initiates the formation of Abeta and therefore is a key drug target for the treatment of AD. The recent generation of BACE1-/- mice by gene targeting in our group has validated BACE1 as the authentic beta-secretase in vivo. In AD, amyloid plaques are associated with a focal inflammatory response that involves activated glia. Inflammatory markers are dramatically elevated in the brains of AD patients and amyloid plaque-developing APP transgenic mice. IL-1beta is a major cytokine released during AD, and recent studies demonstrate that IL-1beta increases the synthesis of APP in cultured astrocytes. Moreover, in APP transgenic mice, activated astrocytes around plaques express BACE1. These data suggest that activated astrocytes express both APP substrate and BACE1 enzyme and thus may produce significant amounts of Abeta. Our hypothesis is that activated astrocytes surrounding amyloid plaques exacerbate plaque development by generating Abeta during AD inflammation. This hypothesis is supported by evidence that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of AD, and that the NSAID ibuprofen inhibits amyloid plaque development in APP transgenic mice. The long-term goal of this project is to understand the role of activated astrocytes in Abeta production and amyloid plaque development. The Specific Aims are the following: 1.) Determine whether BACE1 and APP levels are increased in activated astrocytes and, if so, whether activated astrocytes exhibit increased Abeta production and contribute to amyloid deposition; 2.) Determine whether IL-1beta causes increases in APP and BACE1 synthesis and Abeta production in astrocytes and neurons in vitro and in vivo, and facilitates amyloid deposition in vivo. We will use cultured mouse astrocytes and transgenic and knockout mice as our main model systems for this project. Our analytical approaches will include a combination of molecular (Northern, Western, immunoprecipitation, ELISA) and cellular (immunohistochemistry/light microscopy, immunofluoescence/confocal microscopy) techniques. Importantly, we will develop novel APP transgenic models and use the IL-1beta pellet implantation model of Griffin and colleagues in this project. We anticipate that these studies will provide critical insight into the role of astrocytes and BACE1 in Abeta generation and amyloid deposition, mechanisms that are central to AD pathophysiology. |
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2007 — 2019 | Vassar, Robert J | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Molecular Neuropathology and Mechanisms of Bace1 Elevation in Alzheimer's Disease @ Northwestern University At Chicago ? DESCRIPTION (provided by applicant): BACE1 is the ß-secretase enzyme that initiates Aß production and is a prime therapeutic target for AD. Drugs that inhibit BACE1 enzyme activity are in clinical trials for AD, however the safety and efficacy of these agents are unknown. Recent studies suggest that BACE1 inhibition may cause multiple neurological side effects. Thus, it is crucial to develop alternative therapeutic strategies that reduce BACE1 cleavage of APP without impairing essential BACE1 functions. We have shown that global BACE1 protein levels are markedly elevated in APP transgenic mouse and AD brains. Elevated BACE1 is concentrated within dystrophic axons and terminals surrounding amyloid plaques and is associated with increased generation of BACE1- cleaved APP fragments and Aß42. We also find that Aß42 causes increased resting [Ca2+]i and microtubule disruption in neurons. We hypothesize a feed-forward mechanism in which plaque-associated Aß causes axonal dystrophy, BACE1 accumulation, and accelerated Aß generation that drives AD progression. Elucidating the molecular and cellular mechanisms of dystrophic BACE1 elevation could lead to novel AD therapeutic strategies to normalize BACE1 levels and reduce peri-plaque Aß production, yet preserve BACE1 activity for essential functions and side effect mitigation. We hypothesize that Aß-induced Ca2+ influx into peri-plaque axons causes microtubule disruption, impaired axon transport, BACE1 accumulation, axonal dystrophy, and accelerated Aß generation and amyloid load. Our preliminary data show that Aß elevates resting [Ca2+]i in primary neurons via Ca2+-selective channels. Moreover, axons of Aß-treated primary neurons exhibit disrupted microtubules and impaired BACE1 axon transport. Peri-plaque dystrophic axons in 5XFAD mice also show elevated resting [Ca2+]i and disrupted microtubules. Using Ca2+ channel inhibitors or shRNA-AAVs, we will identify the channel(s) that mediates Aß-induced Ca2+ influx in neurons in vitro and in vivo (Aim 1). Additionally, using Ca2+ channel inhibitors or shRNA-AAVs, we will decrease Aß-induced elevated resting [Ca2+]i, block microtubule and motor protein disruption, improve axon transport, and reduce BACE1 elevation (Aim 2). We will also rescue BACE1 elevation and axon transport by exposing Aß-treated primary neurons and 5XFAD mice to the microtubule stabilizing agent Epothilone D and determine whether Aß-induced BACE1 elevation is tau-independent (Aim 2). Finally, we will determine whether BACE1 elevation accelerates Aß generation and amyloid progression by performing 1) 35S-metabolic labeling of Aß-treated primary neurons to measure de novo Aß production, 2) in vivo Aß microdialysis to analyze Aß production in peri-plaque regions, 3) multicolor Aß time-stamp labeling to analyze the rate of individual plaque growth and dystrophic neurite formation in 5XFAD mice (Aim 3). These experiments will provide proof of concept for therapeutic strategies to reduce peri-plaque BACE1 elevation as a safer alternative to direct inhibition of BACE1 enzyme activity. |
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2016 | Vassar, Robert J | R13Activity Code Description: To support recipient sponsored and directed international, national or regional meetings, conferences and workshops. |
2nd Kloster Seeon Meeting On Bace Proteases in Health and Disease @ Northwestern University At Chicago Project Summary Compelling genetic, biochemical, cell biological, animal model, and human studies suggest that cerebral accumulation of the ?-amyloid peptide (A?) has a critical early role in Alzheimer's disease (AD) pathogenesis. The ?-secretase enzyme BACE1 is the rate-limiting enzyme for A? production. Thus, BACE1 is a prime therapeutic target for the treatment or prevention of AD. Several BACE1 inhibitor drugs for AD are in clinical trials, but the safety and efficacy of these agents are unknown. The BACE proteases field comprises very active and diverse areas of research that have high impact on therapeutic approaches to treat and prevent AD. Here, I propose the 2nd Kloster Seeon Meeting on BACE Proteases in Health and Disease, September 25-27, 2016, in Bavaria, Germany, which has the following objectives: 1) disseminate the latest information on BACE proteases research and catalyze discussion among scientists in academia and industry, 2) promote the training of young scientists, and 3) publish a state-of-the-art review of BACE research to help advance the field and facilitate the development of safe and effective BACE inhibitor drugs for AD. The Scientific Program consists of: 1) a Keynote Lecture by Dr. Kari Stefansson (DeCode Genetics), who recently discovered a mutation in APP that protects against AD by reducing BACE1 cleavage, thus providing proof of concept for therapeutic BACE1 inhibition, 2) two full days of sessions comprising 25-minute talks from 24 leading experts in the BACE proteases field, 3) a session of 2-minute flash talks given by 10 selected graduate students and post-doctoral researchers to introduce their posters, 4) poster sessions on each of two evenings that will enhance the training experience of students and post-docs, 5) a panel discussion between academic and industry scientists on the current state of BACE research and drug development, 6) a conclusion and summary session to remark on the meeting and discuss the direction forward for the field. This meeting is co-organized by Drs. Stefan Lichtenthaler (Technical University Munich) and Robert Vassar (Northwestern University), two leading scientists in the BACE proteases field. The 1st Kloster Seeon Meeting on BACE Proteases in Health and Disease was held at the same location on October 6-8, 2013, and was objectively successful at disseminating the latest BACE research and catalyzing discussion among BACE scientists. Three years have passed, and significant advances in BACE research have been made, including new clinical trials, discoveries of novel BACE1 substrates and functions, different mechanisms of BACE regulation in health and dysregulation in AD, and identification of new proteolytic activities. Given these new advances, the 2nd Kloster Seeon Meeting on BACE Proteases in Health and Disease is timely and important for dissemination of the latest information in the field. Additionally, no other scientific meeting or conference focuses exclusively on BACE proteases research, making this meeting a unique scientific forum that will contribute significantly to the advancement of the AD research and drug development fields. |
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2017 — 2021 | Disterhoft, John F [⬀] Vassar, Robert J |
T32Activity Code Description: To enable institutions to make National Research Service Awards to individuals selected by them for predoctoral and postdoctoral research training in specified shortage areas. |
Predoctoral and Postdoctoral Training Program in Aging and Dementia @ Northwestern University At Chicago Abstract This proposal is a request for continued funding of a broadly based predoctoral and postdoctoral Mechanisms of Aging and Dementia Training Program from the Northwestern University Interdepartmental Neuroscience Program (NUIN). Funding to support four advanced predoctoral candidates, after they have begun full-time thesis research, and four postdoctoral trainees in early or later stages of training, is requested. Training duration will be for two years with a goal to assist trainees in submitting and obtaining support from individual research fellowships following training grant support. This training program developed from a multidisciplinary group of investigators whose work focuses on the mechanisms of aging and dementia, including Alzheimer's Disease, Parkinson's Disease and Amyotrophic Lateral Sclerosis, with approaches spanning molecular, cellular, systems, behavioral, neuropsychological and clinical neuroscience. These faculty are affiliated primarily with NUIN and the Cognitive Neurology and Alzheimer's Disease Center, which has an NIA supported Alzheimer's Disease Center grant, and the Udall Parkinson's Disease Center. The program will be directed by John Disterhoft, PhD and Robert Vassar, PhD in a Multi-PI format, with Dr. Disterhoft directing the program in funding years 16-17, Drs. Disterhoft and Vassar jointly directing the program in funding years 18-19, and Dr. Vassar directing the program in funding year 20. They will have the assistance of Sandra Weintraub, PhD (Associate Director), an internal Steering Committee and an External Advisory Committee. The four predoctoral and four postdoctoral trainees will conduct their research under the guidance of 36 preceptors from 13 departments of 3 schools on the Chicago and Evanston campuses of Northwestern University, and one from Rush University Medical School. Predoctoral trainees will be selected from NUIN and the other participating PhD programs on the basis of course performance, research rotation evaluations, and the relevance of proposed dissertation research. Postdoctoral trainees will be selected on the basis of previous training and a research plan. Special consideration will be given to trainees whose research plans are interdisciplinary and carried out in more than one preceptor laboratory. A concerted effort will be made to recruit trainees from underrepresented backgrounds. The program will offer a broad range of interdisciplinary research and training opportunities in both the fundamental and clinical approaches to aging and dementia research. The preceptor faculty will assist and monitor trainee progress through formal advising and evaluations, through the classroom and through informal discussions. In addition to providing research training, the program will help trainees develop skills in written and oral communication, grant writing, networking, career development and techniques for insuring reproducibility and accuracy of research findings. Instilling a clear awareness of ethical issues facing neuroscientists and responsible conduct in science will be another training goal. |
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2018 | Vassar, Robert J | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Molecular and Cellular Mechanisms of the Unc5c Netrin Receptor in Alzheimer's Disease Pathogenesis @ Northwestern University At Chicago UNC5C is a netrin receptor in which a rare coding mutation, T835M, was recently identified that predisposes to late onset (LO) Alzheimer's disease (AD). Our preliminary suggest that UNC5C T835M causes neuron loss in the presence of A? pathology. We hypothesize that UNC5C T835M predisposes to LOAD by making neurons more vulnerable to cell death induced by pathogenic A? and Tau. We will 1) define cell death pathways in 5XFAD and P301S-Tau mouse models of A? and Tau pathology, respectively, crossed to knockin (KI) mice in which UNC5C T835M is expressed endogenously; 2) identify cell death pathways in human induced pluripotent stem cell (hiPSC) neurons generated from UNC5C T835M patient fibroblasts; 3) use mass spectrometry (MS)-based proteomics to determine the comprehensive UNC5C T835M cell death proteome. In Aim 1, we will determine the molecular mechanism of UNC5C T835M-mediated cell death induced by AD- associated stressors in mouse primary neurons and hiPSC neurons in vitro. We will analyze the cell death pathway induced by A?42 and Tau P301S in UNC5C T835M KI mouse primary neurons and hiPSC neurons derived from human UNC5C T835M patient fibroblasts. Activation of cell death molecules will be assessed using biochemical and cell biological methods. We will attempt to prevent A?- and Tau-induced cell death using pharmacologic inhibition and genetic knockdown of key molecules to validate the cell death pathway in vitro. In Aim 2, we will determine the molecular mechanism of UNC5C T835M-mediated cell death induced by A? and Tau pathologies in vivo. We will analyze cell death in the brains of UNC5C T835M KI mice crossed to 5XFAD and P301S-Tau transgenic mouse models of A? and Tau pathologies, respectively, which also exhibit neuron loss. We predict that UNC5C T835M will decrease the age of onset and increase the severity of cell death in each model. We will assess cell death markers and AD pathologies using biochemical, histological, and behavioral methods. We will attempt to prevent cell death in each model using pharmacologic inhibition and genetic knockdown of key molecules to validate the cell death pathway in vivo. In Aim 3, we will identify the UNC5C T835M cell death pathway proteome induced by pathogenic A? and Tau using unbiased proteomics. We will perform multiplexed quantitative tandem MS-based proteomic analysis of cell extracts from UNC5C T835M and repaired isogenic hiPSC neurons exposed to A?42 or Tau P301S-AAV to define the hiPSC neuron cell death proteome. We will also use tandem MS to identify the cell death proteome in brains of UNC5C T835M KI/5XFAD and KI/P301S-Tau transgenic mice relative to control brains from mice metabolically labeled with 15N. Hits will be prioritized according to potential druggability, validated by immunoblot and immunohistochemistry, and targeted for genetic knockdown in 5XFAD or P301S-Tau mice to potentially prevent neuron loss. These Aims are expected to provide proof of concept for therapeutic targeting of the UNC5C pathway for prevention of neuron loss in AD. |
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2018 — 2019 | Sadleir, Katherine R. Vassar, Robert J |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
A Test of the Calcium Hypothesis of Alzheimers Disease @ Northwestern University At Chicago The calcium hypothesis of Alzheimer's disease (AD) posits that dysregulation of calcium homeostasis is the point of convergence of the many factors risk factors and molecular mechanisms that lead to development of AD and its associated neurodegeneration. A corollary of the calcium hypothesis of AD is that restoration of calcium homeostasis will ameliorate AD pathophysiology and reverse neuronal dysfunction. Surprisingly, despite being nearly 3 decades old, this hypothesis has not been definitively tested in vivo. We propose to directly test the calcium hypothesis by normalizing resting free intracellular calcium levels through exogenous expression of the simple calcium buffer proteins calbindin-D9k and parvalbumin-? in the brains of 5XFAD mice, a model of amyloid pathology in AD. In Aim 1, we will determine if reduced resting free calcium cures the dystrophic axons and neurites that develop around plaques and likely contribute to neuronal dysfunction and increased amyloid generation In Aim 2, we will determine if increasing calcium buffering in the brains of amyloid plaque-containing 5XFAD mice can restore electrophysiological and cognitive impairments. Two adeno-associated viruses will be co-injected into the ventricles of postnatal P0 mouse pups, resulting in viral transduction throughout the brain and lifelong transgene expression. One virus expresses the calcium sensor GCaMP6f from the calmodulin kinase II (CaMKII) promoter, which drives expression in the excitatory neurons of the forebrain. The second virus co-expresses mCherry and a calcium buffer protein (either calbindin-D9k or parvalbumin-?) under the control of a tetracycline-off (TetO) promoter. In mice that express the tetracycline transactivator protein (tTA) under the control of a CaMKII promoter, the calcium buffer protein and mCherry will be expressed in the same population of cells as the calcium sensor GCaMP6f in the absence of the tetracycline analog doxycycline (dox). The pregnant mothers and offspring will be fed dox-containing chow until 6 months of age while the plaques develop. Mice will then be implanted with a cranial window to allow repeated in vivo multiphoton imaging of calcium levels, as measured by GCaMP6f fluorescence, in the dystrophic neurites around plaques. After baseline calcium levels have been measured, we will discontinue the dox diet to induce calcium buffer protein expression and monitor calcium levels and dystrophies by multiphoton microscopy for several weeks. Four weeks after induction, memory performance will be assessed in the Morris water maze, fear conditioning and the Y-maze, hippocampal memory tasks in which the 5XFAD mouse is impaired. At the end of behavioral testing, electrophysiology will be performed to measure the afterhyperpolarization (AHP), which is increased in aged 5XFAD mice and correlates with impaired memory. We predict that increased calcium buffering will ?heal? the dystrophic neurites and improve electrophysiological and cognitive functions, providing strong support for the calcium hypothesis, and validate the use of calcium- reducing therapeutics in AD. |
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2019 — 2020 | Vassar, Robert J | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
Alzheimer's Disease Core Center @ Northwestern University At Chicago PROJECT SUMMARY ? OVERALL COMPONENT The Northwestern ADC is in its 20th year. This renewal application describes the progress of the past cycle and a plan of action for the next 5 years, during which we will pursue the following principal goals: A) Support innovative research at Northwestern University on the biology, early diagnosis, risk factors, and treatment of dementias by bringing together basic and clinical investigators. B) Participate in national collaborations that leverage the strengths of the NIA Centers by using the UDS, transmitting data to NACC, and participating in ADNI, ADCS, NCRAD, LOAD and ADGC. C) Serve a leadership role in FTLD neuropathology, primary progressive aphasia (PPA) and unusually successful brain aging in keeping with the unique strengths of the Northwestern ADC in this area of aging and dementia research. D) Train fellows and junior faculty and attract new investigators to dementia research through accredited clinical fellowships and training grants. E) Ensure that patients, families, and underserved populations are beneficiaries of relevant advances through education, outreach, and novel life enrichment programs. The cores of the ADC are configured to serve the specific goals listed above. The Administrative Core will be responsible for the clinical, scientific and fiscal leadership of the entire ADC, as well as the coordination with national consortia and the selection of projects for pilot funding. The Clinical Core will maintain a cohort of characterized subjects recruited to address ongoing research priorities. The Data Management and Statistics Core will ensure that the data are stored in ways that maximize collaboration and that biostatistic analysis plays a key role in the design and interpretation of research. The Neuropathology Core will characterize patients who come to autopsy according to up-to-date criteria, and distribute tissue, slides, DNA, and data for local and national collaborations. The Outreach and Recruitment Core will work with the Clinical Core to enhance subject recruitment into the ADC, and will develop innovative life enrichment programs to serve patients and their families. The Research Education Component will oversee diversity recruitment for researchers and junior faculty and will coordinate training requirements for the Responsible Conduct of Research. The Executive Committee, composed of all key personnel, will formulate Center priorities based on local and national mandates and will review requests for patients, controls, tissue, and data according to these priorities. |
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2021 | Vassar, Robert J | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
@ Northwestern University At Chicago PROJECT SUMMARY - ADMINISTRATIVE CORE The ultimate goal of an Alzheimer's Disease Research Center (ADRC) is to promote innovative research on dementia and its treatments while ensuring that patients and caregivers become the beneficiaries of resultant advances. An effective Administrative Core is essential for transforming these goals into accomplishments. To this end, the Administrative Core of the Northwestern ADRC will be guided by the following goals: 1) Lead the day-to-day running of the ADRC and promote centerness so that ADRC components function cohesively and leverage dementia-related activities throughout Northwestern University. 2) Maximize the utilization of ADRC resources to fit local and national priorities. 3) Coordinate the adoption of UDS-3, the FTLD module, new clinical trials, and the increased emphasis on biomarkers, including structural and molecular imaging. 4) Facilitate interactions with NACC, NCRAD, and national consortia such as ADNI and ADCS, the Alzheimer's Association, and relevant agencies within the City of Chicago and State of Illinois. 5) Encourage innovative Development Projects, coordinate their review, and monitor the progress of those that receive ADRC funding. To fulfill these goals, the Administrative Core will oversee the finances of the parent NIA P30 and of additional contracts related to multi-center collaborations and clinical trials. It will be responsible for timely progress reports related to these activities as well as the organization of the yearly Scientific Advisory Board (SAB) meeting. An equally important role will be to ensure that the ADRC as a whole meets all IRB and HIPAA requirements and that it is in compliance with NIH policies for human subjects, animal welfare, scientific integrity, data and sample sharing and financial policy. The Administrative Core is also responsible for coordinating the interactions of the ADRC with NIA, other NIH components, other ADRCs, and relevant agencies at the national, state and local levels. Within Northwestern University, the Administrative Core will advocate the allocation of additional faculty, space and financial resources to dementia research. |
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2021 | Vassar, Robert J | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
Northwestern Alzheimer's Disease Research Center @ Northwestern University At Chicago PROJECT SUMMARY - OVERALL COMPONENT The Northwestern ADRC is in its 25th year. This renewal application describes the progress of the past cycle and a plan of action for the next 5 years, during which we will pursue the following principal goals: 1) Support innovative research at Northwestern University on the biology, early diagnosis, risk factors, and treatment of dementias by bringing together basic and clinical investigators. 2) Participate in national collaborations that leverage the strengths of the NIA Centers by using the UDS-3 and FTLD Module and transmitting data to NACC, and participating in ADNI, ADCS, NCRAD, LOAD, ADGC, and FTLD-related consortia. 3) Serve a leadership role in FTLD neuropathology, primary progressive aphasia (PPA), dementias associated with TDP-43 pathology, mid-life onset AD (MOAD), microglia and neuroinflammation, and unusually successful brain aging (SuperAging) in keeping with the unique strengths of the Northwestern ADRC in this area of aging and dementia research. 4) Train fellows and junior faculty and attract new investigators to dementia research through accredited clinical fellowships, Development Project awards, and training grants. 5) Ensure that patients, families, and underserved populations are beneficiaries of relevant advances through education, outreach, and novel life enrichment programs. The cores of the ADRC are configured to serve the specific goals listed above. The Administrative Core will be responsible for the clinical, scientific and fiscal leadership of the entire ADRC, as well as the coordination with national consortia and the selection of Development Projects. The Clinical Core will maintain a cohort of well- characterized subjects recruited to address ongoing research priorities. The Data Management and Statistics Core will ensure that the data are stored in ways that maximize collaboration and that biostatistical consultation plays a key role in the design and interpretation of research. The Neuropathology Core will characterize patients who come to autopsy according to up-to-date criteria, and distribute tissue, slides, DNA, and data for local and national collaborations. The Outreach, Recruitment and Engagement Core will work with the Clinical Core to enhance participant recruitment and retention in the ADRC, and will develop innovative life enrichment programs to serve patients and their families. The Research Education Component will oversee diversity recruitment for researchers and junior faculty and coordinate training requirements for the Responsible Conduct of Research. The Imaging Biomarker Core will perform up-to-date multimodal neuroimaging of Clinical Core participants, including amyloid and tau PET. The Executive Committee, composed of all key personnel, will formulate ADRC priorities based on local and national mandates and will review requests for patients, controls, tissue, and data. |
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