REGENERATIVE RESEARCH FOUNDATION

LLCNGSLHHLJ5

4S6G0

2026-04-22

http://www.neuralsci.org

2025-04-28

2007-06-01

4S6G0

Active

Non-Manufacturer

2025-04-28

2030-04-28

2026-04-22

TOM IRWIN

http://www.neuralsci.org

203654626

2024

51

5186948188

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2023

47

5186948188

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2022

44

5186948188

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2021

38

5186948188

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2020

38

5186948188

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HHSN263201000954P

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AWARD

PO

45000.00

45000.00

45000.00

Department of Health and Human Services

2010-08-16

T25 FLASK OF HUMAN IPS DERIVED RPE CELLS (STANDING ORDER , 1 FLASK PER MONTH) LAB POC SHELDON MILLER

424210: DRUGS AND DRUGGISTS' SUNDRIES MERCHANT WHOLESALERS

6505: DRUGS AND BIOLOGICALS

2025-05-30

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Department of Health and Human Services

IPSC-BASED MODEL TO STUDY FRONTOTEMPORAL DEMENTIA DUE TO MAPT MUTATION - OUR GOAL IS TO GENERATE AND VALIDATE A NOVEL, CELLULARLY COMPLEX MODEL OF FRONTOTEMPORAL DEMENTIA (FTD) DUE TO MUTATIONS IN THE MAPT GENE THAT ENCODES TAU (FTD-TAU). THE NINDS 2022 ADRD SUMMIT REPORT DESCRIBES THE NEED FOR SUCH A MODEL. OVER 50 MUTATIONS IN MAPT CAUSE FTD-TAU, WHICH MANIFESTS BY ABNORMAL TAU ACCUMULATION IN SUBSETS OF CEREBRAL CORTICAL NEURONS, ASTROCYTES, AND OLIGODENDROCYTES. THIS LEADS TO CELLULAR DYSFUNCTION AND DEATH, PRIMARILY IN THE FRONTAL AND TEMPORAL CORTICAL REGIONS, LEADING TO DEFICITS IN EXECUTIVE FUNCTION, LANGUAGE, AND BEHAVIORAL RESPONSES. MAPT MUTATION CARRIERS FREQUENTLY ALSO HAVE SIGNIFICANT DEGENERATION OF SUBCORTICAL AREAS, INCLUDING THE STRIATUM AND THE MIDBRAIN DOPAMINERGIC SUBSTANTIA NIGRA (SNC) AND MIDBRAIN VENTRAL TEGMENTAL AREA (VTA) NEURONS, CONTRIBUTING TO PARKINSONISM AND BEHAVIORAL CHANGES. HENCE THERE IS NEED TO MODEL MULTIPLE BRAIN AREAS TO MORE FULLY CAPTURE BRAIN CELL VULNERABILITY. FURTHERMORE, THERE ARE EXTENSIVE CONNECTIONS BETWEEN THESE MIDBRAIN AND FOREBRAIN AREA NEURONS THAT ARE AFFECTED IN FTD- TAU, WHICH IMPLICATES THIS CIRCUITRY IN PATHOLOGY DEVELOPMENT AND SPREAD. PRIOR 3D HUMAN CELL MODELS OF FTD- TAU HAVE FOCUSED ON THE CEREBRAL CORTEX NEURONS AND GLIA, WHICH DEMONSTRATE KEY FEATURES OF CORTICAL TAUOPATHY, INCLUDING ACCUMULATION OF ABNORMALLY PHOSPHORYLATED TAU AND DEGENERATION OF GLUTAMATERGIC NEURONS. HERE, WE PROPOSE TO BUILD A MODEL OF AXON-CONNECTED 3D CEREBRAL CORTEX, STRIATUM, AND MIDBRAIN ORGANOIDS THAT INCORPORATES THE MAJOR CELL TYPES AND RECONSTRUCTS KEY ELEMENTS OF THE FOREBRAIN-MIDBRAIN CIRCUITY AFFECTED IN FTD-TAU. TO FURTHER ADVANCE THE MODEL AND INCLUDE CRITICAL CELL TYPES IMPLICATED IN FTD-TAU, IT WILL INCORPORATE MICROGLIA. THE GOAL IS A HUMAN CELL MODEL OF AFFECTED BRAIN REGIONS THAT EXHIBITS IMPROVED CONSTRUCT AND FACE VALIDITY OVER EXISTING MODELS. IN AIM 1 WE WILL DEVELOP AND OPTIMIZE PRODUCTION AND CONNECTIVITY OF THE CORTICAL- STRIATAL-MIDBRAIN (COST-MB) MODEL. IN AIM 2 WE WILL GENERATE COST-MB MODELS FROM DIFFERENT MAPT MUTATIONS VS ISOGENIC CONTROL LINES. WE WILL DEEPLY PHENOTYPE THE MODELS AND COMPARE THEM TO PATIENT BRAIN SAMPLES WITH MAPT MUTATIONS IN FACE AND CONSTRUCT VALIDATION STUDIES. QUANTITATIVE METRICS WILL BE USED TO ASSESS REPRODUCIBILITY OF THE MODEL AND ITS PHENOTYPIC RESEMBLANCE TO PATIENT FOREBRAIN AND MIDBRAIN PATHOLOGY. WE WILL DEMONSTRATE INDEPENDENT REPLICATION OF THE MODEL IN MORE THAN ONE INSTITUTION LAB TO DEMONSTRATE ROBUSTNESS. TRANSPARENT SHARING OF DETAILED PROTOCOLS AND DATA WILL AID ADOPTION OF THE COST-MB FTD-TAU MODEL. THE MODEL WILL BE GENERATED USING OUR COLLECTION OF HUMAN INDUCED PLURIPOTENT STEM CELL (IPSC) LINES WITH MAPT MUTATIONS IN CODING AND NON-CODING REGIONS THAT AFFECT BOTH FOREBRAIN AND MIDBRAIN PATHOLOGY AND CRISPR-CORRECTED ISOGENIC CONTROL LINES; THESE LINES ARE FULLY AVAILABLE TO OTHER RESEARCHERS. THE COST-MB MODEL CAN BE USED IN THE FUTURE TO STUDY DISEASE MECHANISMS AND DEVELOP THERAPEUTICS TO COMBAT FTD-TAU AND POTENTIALLY OTHER TAUOPATHIES OR RELATED NEURODEGENERATIVE DISEASES THAT CAUSE MULTI-REGION BRAIN CELL LOSS.

1540579.00

0.00

0.00

2024-08-15

View on USAspending

Department of Health and Human Services

HUMAN IPSC MODEL OF CEREBRO-VASCULAR INTERACTIONS IN ADRD - WE PROPOSE TO GENERATE AND VALIDATE A NOVEL MODEL THAT INCORPORATES HUMAN CEREBRAL CORTICAL NEURONS AND GLIA, VASCULAR ENDOTHELIAL CELLS, NEURAL CREST PERICYTES AND MICROGLIA FROM HUMAN INDUCED PLURIPOTENT STEM CELLS (IPSCS). THE GOAL IS A MODEL WITH IMPROVED CONSTRUCT, FACE, AND PREDICTIVE VALIDITY TO STUDY THE CEREBRO-VASCULAR INTERACTIONS COMMON TO ALZHEIMER’S DISEASE-RELATED DEMENTIAS (ADRD). THE NINDS 2022 ADRD SUMMIT REPORT DESCRIBES THE NEED FOR SUCH A MODEL. IN PRIOR STUDIES WE DEVELOPED A REPRODUCIBLE HUMAN 3D CEREBRAL CORTEX ORGANOID MODEL TESTED ACROSS 63 IPSC LINES WITH 90% SUCCESS. IT IMPROVED EFFICIENCY IN ORGANOID PRODUCTION FROM 10% TO APPROACHING 100%. ORGANOIDS GROWN WITH THE PROTOCOL HAVE UNIFORM SIZE, SHAPE, PREDICTABLE GROWTH CURVES AND CELL COMPOSITION. SINGLE CELL TRANSCRIPTOME STUDIES DEMONSTRATE HIGH OVERLAP BETWEEN IPSC LINES FROM DIFFERENT DONORS, AN IMPORTANT ADVANCE FOR STUDIES OF BOTH GENETIC AND SPORADIC DISEASE. WE ALSO RECENTLY DEVELOPED AN IPSC-DERIVED 3D VASCULATURE MODEL FORMING ROBUST, VESSEL-LIKE STRUCTURES OF ENDOTHELIAL CELLS AND PERICYTES IN AN INERT HYDROGEL. PRELIMINARY STUDIES DEMONSTRATE THAT THESE TWO ADVANCED MODELS CAN BE INTEGRATED TO GENERATE A HUMAN CELL 3D CEREBRO-VASCULAR MODEL. IN AIM 1, THE R61 PHASE, WE WILL OPTIMIZE THE INCORPORATION OF THESE TWO MODELS TO ACHIEVE GREATEST REPRODUCIBILITY OF CELL COMPOSITION REFLECTING VASCULARIZED CEREBRAL CORTICAL TISSUE IN VIVO. THE MODEL WILL BE GENERATED FROM AT LEAST THREE DIFFERENT PSEN1 MUTATION IPSC LINES VERSUS HEALTHY CONTROLS. THERE IS SIGNIFICANT NEED FOR THIS MODEL GIVEN THAT CURRENT PSEN1 MUTATION TRANSGENIC AND KNOCK-IN MOUSE MODELS LACK SEVERAL KEY FEATURES OF NEURO- AND VASCULAR PATHOLOGY SEEN IN HUMAN DISEASE. QUANTITATIVE METRICS WILL BE USED TO ASSESS EFFICIENCY AND REPRODUCIBILITY OF THE MODEL AND ITS ABILITY TO REPRODUCE PSEN1 MUTATION CORTICAL PATHOLOGY, INCLUDING CEREBRAL AMYLOID ANGIOPATHY (CAA). WITH THE ACHIEVEMENT OF PROSPECTIVELY DETERMINED QUANTITATIVE CRITERIA, WE WILL ADVANCE TO THE R33 PHASE OF THE PROJECT. IN AIM 2, THE PSEN1 MUTATION MODELS WILL BE EXAMINED FOR FACE, CONSTRUCT, AND PREDICTIVE VALIDITY. THIS PHASE WILL INCLUDE COLLABORATORS WITH EXPERTISE IN EXAMINING PSEN1 MUTATION CARRIER TISSUE PATHOLOGY, BRAIN SINGLE NUCLEAR TRANSCRIPTOMES, METABOLOMICS, LIPIDOMICS, AND CEREBROSPINAL FLUID (CSF) COMPOSITION. WE WILL ASSESS ESTABLISHED CHARACTERISTICS OF PSEN1 MUTATION-INDUCED CEREBRAL PATHOLOGY, SUCH AS ALTERED EXPRESSION OF A40,42 AND 43, AND TAU. VALIDATION TESTS WILL INCLUDE THOSE USED FOR CLINICAL EVALUATION WHERE TEST SENSITIVITY, DYNAMIC RANGE AND PREDICTIVE VALUE ARE KNOWN. THE PREDICTIVE VALIDITY OF THE MODEL WILL BE ASSESSED BY COMPARING PSEN1 MUTATION TO GENETIC CONTROLS, INCLUDING CRISPR ENGINEERED ISOGENIC CONTROL LINES. IN ADDITION, WE WILL ASSESS THE IMPACT OF ANTIBODY THERAPIES THAT ARE APPROVED FOR PSEN1 MUTATION CARRIERS, TO DETERMINE WHETHER THEY CAN BIND A SPECIES, OFFSET OTHER SIGNS OF PATHOLOGY, AND OFFER INSIGHT PERTINENT TO DRUG-RELATED VASCULAR SIDE-EFFECTS. WE WILL DEMONSTRATE INDEPENDENT REPLICATION OF THE MODEL IN A DIFFERENT INSTITUTION LAB TO DEMONSTRATE ROBUSTNESS. TRANSPARENT SHARING OF DETAILED PROTOCOLS AND DATA WILL AID ADOPTION OF THE MODEL.

1931965.00

0.00

0.00

2023-03-17

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Department of Health and Human Services

HIGH-DENSITY MICROELECTRODE ARRAY - PI: KIEHL, THOMAS R. , REGENERATIVE RESEARCH FOUNDATION, HIGH-DENSITY MICROELECTRODE ARRAY SUMMARY/ABSTRACT WITH THIS APPLICATION, WE REQUEST FUNDING TO PROCURE THE HYPERCAM ALPHA PLATFORM FROM 3BRAIN AG (ZÜRICH SWITZERLAND). THE HYPERCAM ALPHA IS A MULTI-WELL, HIGH-DENSITY MICROELECTRODE ARRAY SYSTEM FOR OBSERVING AND STIMULATING IN VITRO ELECTROPHYSIOLOGICAL ACTIVITY IN ELECTRO-ACTIVE CELL CULTURES, CELL CONSTRUCTS, ORGANOIDS, AND PRIMARY TISSUE SAMPLES. THIS INSTRUMENT PROVIDES SEVERAL KEY FEATURES: 1) HIGH-RESOLUTION RECORDING CAPABILITY; 2) DYNAMIC STIMULATION FUNCTIONALITY, 3) A MULTI-WELL FORMAT; 4) 3D SENSOR OPTIONS, AND 5) SOPHISTICATED ANALYSIS SOFTWARE. THESE FEATURES ENSURE ITS UTILITY ACROSS A RANGE OF BIOLOGICAL INVESTIGATIONS TO MEET THE HIGH-THROUGHPUT AND HIGH-FIDELITY DEMANDS OF OUR USERS AND COLLABORATORS. THIS SUBMISSION ADDRESSES A SIGNIFICANT UNMET NEED IN OUR INSTITUTE AND REGION, NAMELY THE ABILITY TO TEST THE FUNCTIONAL IMPACT OF CELLULAR INTERACTIONS, GENETIC CHANGES OR OF PERTURBAGENS ON NEURAL SYSTEMS AT SCALE. THE RESEARCHERS IDENTIFIED IN THIS SUBMISSION (SPANNING FIVE INSTITUTIONS) ARE ENGAGED IN THE STUDY OF A WIDE RANGE OF NEUROLOGICAL DISFUNCTION FROM DISEASE, AGING, INJURY AND DEVELOPMENTAL DISORDERS. PLACEMENT OF THIS INSTRUMENT WILL DIRECTLY ADVANCE WORK IN FRONTOTEMPORAL DEMENTIA, ALZHEIMER’S, VASCULAR CONTRIBUTIONS TO DEMENTIA, SEX- SPECIFIC AGING IMPACT ON COGNITIVE FUNCTION, TISSUE REGENERATION, SPINAL CORD INJURY, BRAIN DEVELOPMENT, AND DISEASE IMPACT ON NEUROLOGICAL DEVELOPMENT. THIS INSTRUMENT WILL HELP TO QUANTIFY MODEL SYSTEMS, SUCH AS BRAIN ORGANOIDS, THAT HAVE FAST BECOME THE WORKHORSES OF THE FIELD. PROJECTS DESCRIBED HERE ALSO ADVANCE THE DEVELOPMENT OF NEW, MORE CAPABLE, MODEL SYSTEMS AND EVEN OF NEXT GENERATION MEA-RELATED DEVICES. THE PRIMARY, CONCRETE, LONG-RANGE BENEFIT OF THIS INSTRUMENT TO THE BIOMEDICAL RESEARCH GOALS OF RRF/NSCI/NEURACELL IS TO PROVIDE ROUTINE, CLEAR, HIGH-RESOLUTION, EASILY CAPTURED, CHARACTERIZATION AND QUANTIFICATION OF THE BEHAVIOR AND FUNCTION OF THE NUMEROUS NEUROLOGICAL SYSTEMS UNDER STUDY AT OUR INSTITUTION. THE USE OF THIS INSTRUMENT WILL BE INTEGRATED INTO NEARLY EVERY RESEARCH PROGRAM WITHIN OUR WALLS. BEYOND OUR ORGANIZATION, THIS INSTRUMENT WILL: AMPLIFY THE EXISTING PROGRAMS OF OUR MAJOR USERS; HELP OUR MINOR USERS ESTABLISH AND GROW THEIR RELATED RESEARCH PROGRAMS; AND ENDOW A FOUNDATION FOR FUTURE TECHNOLOGY DEVELOPMENT.

239841.00

0.00

0.00

2022-02-22

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Department of Health and Human Services

DEVELOPING ANTIBODY-OLIGONUCLEOTIDE BRIDGES TO SIMPLIFY SINGLE CELL SPATIAL TRANSCRIPTOMICS - PROJECT SUMMARY SINGLE CELL RNA-SEQUENCING (SCRNA-SEQ) HAS ENABLED RESEARCHERS TO INVESTIGATE A WIDE ARRAY OF BIOLOGICAL PROCESSES AND HOW TISSUE HETEROGENEITY CONTRIBUTES TO FUNCTION. THESE TECHNOLOGIES HAVE LED TO THE DEVELOPMENT OF PROGRAMS, SUCH AS THE NIH HUMAN BIOMOLECULAR ATLAS PROGRAM, TO UNDERSTAND HOW CELLS INTERACT IN AN ORGANISM TO DRIVE ITS FUNCTION. THE DEVELOPMENT OF SPATIAL TRANSCRIPTOMIC TECHNOLOGIES HAS ALLOWED RESEARCHERS TO INVESTIGATE HOW CELL-CELL INTERACTIONS AFFECT CELLULAR GENE EXPRESSION WITHIN A TISSUE. CURRENT APPROACHES GENERALLY RELY IN SITU RNA BASED METHODOLGIES OR SLIDE-BASED SEQUENCING IN COMBINATION WITH SCRNA-SEQ (E.G. SLIDE-SEQ) TO GENERATE SPATIAL MAPS OF INTERACTING CELLS. THESE TECHNOLOGIES HAVE HELPED DEMONSTRATE THE POWER OF COMBINING THE TISSUES STRUCTURAL DATA WITH TRANSCRIPTIONAL DATA TO BETTER UNDERSTAND CELL BEHAVIOR IN A TISSUE AND GOING FORWARD IMPROVING THE INTERFACE BETWEEN THESE TECHNOLOGIES WILL BE KEY TO UNCOVERING HOW STRUCTURE AND CELL TRANSCRIPTION DRIVES FUNCTION. HOWEVER, MULTIPLE BARRIERS IMPEDE THE WIDESPREAD ADOPTION OF THE CURRENT METHODS FOR PERFORMING SPATIAL TRANSCRIPTOMICS, INCLUDING SIGNIFICANT FINANCIAL COST, TIME REQUIREMENTS, AND A LACK OF SUFFICIENT EXPERTISE. HEREIN, WE PROPOSE TO DEVELOP A SIMPLE REAGENT COMPATIBLE WITH CURRENT PROTOCOLS FOR DROP-BASED AND PIPETTE-BASED SCRNA-SEQ TECHNOLOGIES. THIS REAGENT WILL BE ABLE TO GENERATE SPATIAL DATA IN THE NORMAL COURSE OF SCRNA-SEQ EXPERIMENTS WITHOUT SIGNIFICANTLY INCREASING COST OR TIME COMMITMENTS. WE PROPOSE TO INVENT “ANTIBODY-OLIGONUCLEOTIDE BRIDGES” AND BUILD SOFTWARE CAPABLE OF BIOINFORMATICALLY GENERATING A NETWORK OF CELL-CELL CONTACTS ACROSS THE TISSUE TO RECAPITULATE THE SPATIAL RELATIONSHIPS OF THE CELLS IN A TISSUE. IN THIS PROPOSAL, WE WILL CARRY OUT A PROOF-OF- PRINCIPAL EXPERIMENT FOR THE AO BRIDGE SCRNA-SEQ APPROACH FOR GENERATING THE SPATIAL RELATIONSHIPS BETWEEN CELLS.

478500.00

0.00

0.00

2024-08-12

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Department of Health and Human Services

CELL TYPE AND REGIONAL VULNERABILITY IN FRONTOTEMPORAL DEMENTIA - PROJECT SUMMARY/ABSTRACT A KEY QUESTION IN TAUOPATHY RESEARCH IS WHY SOME BRAIN CELL POPULATIONS ARE SIGNIFICANTLY AFFECTED WHILE OTHERS ARE RELATIVELY SPARED. THE LONG-TERM GOAL OF THIS STUDY IS TO UNDERSTAND THIS DIFFERENTIAL CELL VULNERABILITY AND USE THE KNOWLEDGE TO DEVELOP THERAPIES THAT PROTECT NEURAL CELLS FROM TAUOPATHY-RELATED DEGENERATION. MUTATIONS IN THE MAPT GENE THAT ENCODES TAU COMMONLY CAUSE EXTENSIVE PATHOLOGY IN THE FOREBRAIN, WITH SIGNIFICANT LOSS OF FRONTAL AND TEMPORAL LOBE CEREBRAL CORTICAL CELLS LEADING TO BEHAVIORAL, LANGUAGE AND COGNITIVE DEFICITS. HOWEVER, A SUBSET OF MAPT MUTATIONS ALSO CAUSE SIGNIFICANT DEGENERATION OF MIDBRAIN DOPAMINERGIC NEURONS IN THE SUBSTANTIA NIGRA CONTRIBUTING TO A PARKINSONISM PHENOTYPE. FURTHERMORE, THESE CELLS ARE CONNECTED: MIDBRAIN DOPAMINERGIC NEURONS WIDELY INNERVATE THE PREFRONTAL CORTEX AND ARE RECIPROCALLY INNERVATED VIA CORTICO-STRIATAL-NIGRAL CIRCUITS. WHY SPECIFIC MAPT MUTATIONS SIGNIFICANTLY AFFECT THE MIDBRAIN IN ADDITION TO CORTEX WHILE OTHERS DO NOT, AND HOW CONNECTIVITY BETWEEN THESE REGIONS WITH THE POTENTIAL FOR PATHOLOGICAL TAU SPREAD MAY BE INVOLVED, REPRESENT SIGNIFICANT GAPS IN KNOWLEDGE THAT WE WILL ADDRESS IN THIS PROPOSED STUDY. OVER THE PAST FEW YEARS, WE HAVE HELPED CREATE A LARGE IPSC LINE COLLECTION FROM PATIENTS WITH FAMILIAL DEMENTIA DUE TO MUTATIONS IN THE MAPT GENE, INCLUDING ISOGENIC CONTROLS. PHENOTYPIC ANALYSES SHOW MAPT MUTANT AND CONTROL IPSC-DERIVED CEREBRAL CORTICAL CELLS ARE INITIALLY PHENOTYPICALLY SIMILAR BUT DEVELOP DIFFERENCES WITH MATURATION THAT INCLUDE INCREASED TAU AGGREGATION, TAU HYPERPHOSPHORYLATION AND VULNERABILITY TO SEVERAL STRESSORS, ASSOCIATED WITH THE MUTATION. HOWEVER, TO DATE, STUDIES COMPARING FOREBRAIN AND MIDBRAIN CELL POPULATION RESPONSES TO MAPT MUTATIONS THAT DIFFERENTIALLY AFFECT THESE BRAIN REGIONS HAVE NOT BEEN DONE. SUCH COMPARISONS HAVE THE POTENTIAL TO REVEAL COMMON AND UNIQUE MOLECULAR MECHANISMS THAT UNDERLIE CELL VULNERABILITY. OUR APPROACH IS TO USE HUMAN IPSC-DERIVED 3D ORGANOIDS, WHICH RECAPITULATE COMPLEX CELL-CELL INTERACTIONS IN A HUMAN CELL SYSTEM AND ENABLE LONG-TERM CULTURE OVER SEVERAL MONTHS. WE WILL CREATE CORTICAL AND MIDBRAIN ORGANOIDS FROM TWO MAPT MUTATIONS THAT PRIMARILY AFFECT CORTEX AND TWO THAT AFFECT BOTH CORTEX AND MIDBRAIN, VERSUS RESPECTIVE ISOGENIC CONTROLS. IN AIM 1 WE WILL EXAMINE THE IMPACT OF THESE MAPT MUTATIONS ON CELL POPULATIONS AND GENE EXPRESSION OVER TIME USING SINGLE CELL TRANSCRIPTOMICS TO DEFINE HOW DIVERSE CELL TYPES RESPOND TO EACH MUTATION. IN AIM 2, WE WILL CREATE ASSEMBLOIDS OF CORTICAL AND MIDBRAIN ORGANOIDS TO MODEL THE CIRCUITRY BETWEEN THE REGIONS AND DETERMINE WHETHER THIS CONNECTIVITY ALTERS PATTERNS OF CELL VULNERABILITY AND ENABLES THE SPREAD OF PATHOLOGICAL TAU FROM ONE REGION TO ANOTHER, DEPENDING ON SPECIFIC MAPT MUTATION. IN AIM 3 WE WILL PROBE THE IMPACT OF STIMULATING TAU DEGRADATION ON DIFFERENTIAL CELL VULNERABILITY IN CEREBRAL CORTEX AND MIDBRAIN.

1271367.34

0.00

0.00

20-3654626

Government Instrumentality, Title-Holding Corporation, Charitable Organization, Educational Organization, Local Association of Employees, Agricultural Organization, Horticultural Organization, Board of Trade, Business League, Pleasure, Recreational, or Social Club, Fraternal Beneficiary Society, Order or Association, Voluntary Employees' Beneficiary Association (Non-Govt. Emps.), Voluntary Employees' Beneficiary Association (Govt. Emps.), Domestic Fraternal Societies and Associations, Teachers Retirement Fund Assoc., Benevolent Life Insurance Assoc., Mutual Ditch or Irrigation Co., Burial Association, Cemetery Company, Credit Union, Other Mutual Corp. or Assoc., Mutual Insurance Company or Assoc. Other Than Life or Marine, Corp. Financing Crop Operations, Supplemental Unemployment Compensation Trust or Plan, Employee Funded Pension Trust (Created Before 6/25/59), Post or Organization of War Veterans, Legal Service Organization, Black Lung Trust, Multiemployer Pension Plan, Veterans Assoc. Formed Prior to 1880, Trust Described in Sect. 4049 of ERISA, Title Holding Co. for Pensions, etc., State-Sponsored High Risk Health Insurance Organizations, State-Sponsored Workers' Compensation Reinsurance, ACA 1322 Qualified Nonprofit Health Insurance Issuers, Apostolic and Religious Org. (501(d)), Cooperative Hospital Service Organization (501(e)), Cooperative Service Organization of Operating Educational Organization (501(f)), Child Care Organization (501(k)), Charitable Risk Pool, Qualified State-Sponsored Tuition Program, 4947(a)(1) - Private Foundation (Form 990PF Filer)

2007-11

Medical Research: Neurology, Neuroscience Research

Type of organization and use of contribution: A public charity. Deductibility Limitation: 50% (60% for cash contributions)

24

$349,840

2020-04-28

Paid in Full

100

$349,840

Unanswered

Unknown/NotStated

Unanswered

Unanswered

$352,332.01

KeyBank National Association

Payroll: $349,840