HHS Recovery Act Recipient Reporting Readiness Tool
Step 4. Review and Copy the Grant Awards Data
TAGGS provides some – but not all – of the data needed for the Recipient Report. Recipients are responsible for directly collecting and reporting all required data to FederalReporting.gov. Data that HHS does not currently collect are highlighted in yellow. Do not copy this highlighted information. Please enter the appropriate data for your organization in these required fields. For assistance with entering these data please contact FederalReporting.gov.
You may capture the data HHS does provide by copying data from this screen and pasting it into the reporting format of your choice, such as the Excel spreadsheet template, the XML template, or by logging into the online form. For assistance with copying and pasting these data please e-mail our help desk at Readiness Help.
| Recipient Report: Grant or Loan | ||
| Prime Recipient |
| Reporting Information | ||
| Award Type | Award Number | Final Report |
| Grant | 1R21NS056057-01A2 | Recipient responsible for this data |
| Award Recipient Information | ||
| Recipient DUNS Number | Recipient Account Number | Recipient Congressional District |
| 049515844 | Recipient responsible for this data | Not Available |
| Award Information | ||
| Funding Agency Code | Awarding Agency Code | Award Date |
| 7529 | 7529 | 05-01-2009 |
| Amount of Award | Sub Account Number for Program Source (TAS) | |
| $ 191,875 | Recipient responsible for this data | |
| Program Source (TAS)* | CFDA Number | |
| 750901 | 93.701 | |
| Total Number of Sub Awards to Individuals | Total Amount of Sub Awards to Individuals | |
| Recipient responsible for this data | Recipient responsible for this data | |
| Total Number of Payments to Vendors less than $25,000/award | Total Amount of Payments to Vendors less than $25,000/award | |
| Recipient responsible for this data | Recipient responsible for this data | |
| Total Number of Sub Awards less than $25,000/award | Total Amount of Sub Awards less than $25,000/award | |
| Recipient responsible for this data | Recipient responsible for this data | |
| Award Description | ||
| DESCRIPTION (provided by applicant): Excessive activation of ionotropic glutamate receptors increases oxidative stress, which contributes to the neurodegeneration observed following neurological insults such as ischemia and seizures, as well as contributes to neuronal death in neurodegenerative diseases (Alzheimer's, Parkinson's, etc.). From a clinical perspective, it is a clear threat to brain function and to survival. It is believed that generation of reactive oxygen species and ensuing oxidative stress is a major contributor to glutamate toxicity. At the same time, oxidative stress is a major cause of DNA damage, which is also a common component of neuronal injury. DNA damage may contribute to neuronal loss and injury not only after acute brain insults but also under various chronic neurodegenerative conditions, such as Alzheimer's, Huntington's, and Parkinson's diseases, amyotrophic lateral sclerosis, ataxia telangiectasia and many other neurological disorders. The most lethal form of DNA damage, the double strand breaks (DSBs), and the ability of cells to repair them has not yet been directly demonstrated following excessive stimulation of glutamate receptors. While limited evidence suggests the importance of DSBs and their repair machinery in vulnerability to glutamate-induced injury, no systematic direct studies have been done in mature neurons. We have developed a sensitive model to start addressing the role of DSB DNA damage in neuronal vulnerability to glutamate-mediated insults using phosphorylation of histone variant H2A.X, which occurs rapidly following DNA DSBs. Our general working hypothesis is that the consequences of unrepaired DSBs in terminally differentiated neurons are critical contributors to neuronal demise in the aftermath of excessive excitation. Conversely, successful repair of these breaks may increase neuronal survival following glutamate-driven insults. Specific Aims will test the following specific hypotheses aiming at proving this concept: 1) Increased phosphorylation of histone H2AX following activation of ionotropic glutamate receptors will result in increased DSB repair; this hypothesis we will tested by measuring DSB repair activity in rat cortical neuronal cultures; 2) Impairment of H2AX phosphorylation will result in increased glutamate toxicity due to the disruption of the DSB repair pathway. To test this, we will examine vulnerability of neurons from H2AX-/- transgenic mice to vulnerability to glutamate toxicity and evaluate their DSB repair capabilities. We expect that H2AX-/- neurons will be more vulnerable to glutamate toxicity and demonstrate diminished DSB repair as compared to wild-type cells. Moreover, we will reconstitute functional histone H2AX in H2AX-/- neurons using lentiviral expression and evaluate the restoration of their resistance to glutamate toxicity. Testing these hypotheses may reveal a novel common mechanism contributing to neurotoxicity in a variety of neurodegenerative disorders, will lead to identification of attractive new targets for therapy of these disorders, and will lay a foundation for future interventional studies in vivo targeting DSB repair pathway in neurons. PUBLIC HEALTH RELEVANCE: Damage to DNA is a common component of neuronal injury. It may contribute to neuronal loss and injury not only after acute brain insult (e.g., prolonged seizures, stroke, TBI) but also under various chronic neurodegenerative conditions, such as Alzheimer's disease, Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis, ataxia telangiectasia, among other neurological disorders that currently have no effective cure. Excessive excitation also contributes to many of these pathologies and is believed to be the major cause of DNA damage. However, little is known about the mechanisms responsible for the excitation- driven formation of the most lethal type of DNA damage (double strand breaks) in neurons and the ability of nerve cells to withstand this damage. This proposal will examine these mechanisms and will lay the foundation for identification of new targets for therapy of a broad variety of neurological conditions relevant to excitotoxicity. | ||
| Project Information | ||||||||||||||||||||||||||
| Project Name or Project/Program Title |
Project Status | Total Federal Amount ARRA Funds Received/Invoiced |
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| CHROMATIN MODIFICATIONS AND VULNERABILITY TO GLUTAMATE TOXICITY | Recipient responsible for this data | Recipient responsible for this data | ||||||||||||||||||||||||
| Number of Jobs | Description of Jobs Created | |||||||||||||||||||||||||
| Recipient responsible for this data | Recipient responsible for this data | |||||||||||||||||||||||||
| Quarterly Activities/Project Description | ||||||||||||||||||||||||||
| Recipient responsible for this data | ||||||||||||||||||||||||||
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| Total Federal Amount of ARRA Expenditure |
Total Federal ARRA Infrastructure Expenditure |
Infrastructure Contact Name | ||||||||||||||||||||||||
| Recipient responsible for this data | Recipient responsible for this data | Recipient responsible for this data | ||||||||||||||||||||||||
| Infrastructure Contact Email | Infrastructure Contact Phone | Infrastructure Contact Phone Ext. | ||||||||||||||||||||||||
| Recipient responsible for this data | Recipient responsible for this data | Recipient responsible for this data | ||||||||||||||||||||||||
| Infrastructure Contact Street Address 1 | Infrastructure Contact Street Address 2 | Infrastructure Contact Street Address 3 | ||||||||||||||||||||||||
| 37TH & O STREETS, NW | Not Available | Recipient responsible for this data | ||||||||||||||||||||||||
| Infrastructure City | Infrastructure State | Infrastructure ZIP Code+4 | ||||||||||||||||||||||||
| WASHINGTON | DC | 20057 | ||||||||||||||||||||||||
| Infrastructure Purpose and Rationale | ||||||||||||||||||||||||||
| Recipient responsible for this data | ||||||||||||||||||||||||||
| Primary Place of Performance | ||
| Street Address 1 | Street Address 2 | City |
| 3970 RESERVOIR RD, N.W. | Recipient responsible for this data | WASHINGTON |
| State | Zip Code+4 | Congressional District |
| DC | 20057 | Not Available |
| Country | ||
| US | ||
| Recipient Highly Compensated Officers | |||
| Prime Recipient Indication of Reporting Applicability | # | Officer Name | Officer Compensation |
| Recipient responsible for this data | 1 | Recipient responsible for this data | Recipient responsible for this data |
| 2 | Recipient responsible for this data | Recipient responsible for this data | |
| 3 | Recipient responsible for this data | Recipient responsible for this data | |
| 4 | Recipient responsible for this data | Recipient responsible for this data | |
| 5 | Recipient responsible for this data | Recipient responsible for this data | |
This concludes the current search.
To begin a new search, return to the HHS Recovery Act Recipient Reporting Readiness Tool.
USE IN THE RECIPIENT REPORT
The information provided by this tool is baseline data that the Recipient should include in the Recipient Report that must be submitted to FederalReporting.gov beginning October 1, 2009. The data from this tool can be cut and pasted directly into the Recipient Report.
