We 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.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Laura B. Ngwenya is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2003 — 2005 |
Ngwenya, Laura |
F31Activity Code Description: To provide predoctoral individuals with supervised research training in specified health and health-related areas leading toward the research degree (e.g., Ph.D.). |
Minority Predoctoral Fellowship Program @ Boston University Medical Campus
[unreadable] DESCRIPTION (provided by applicant): Using a non-human primate model of normal aging, this investigation will explore the role of adult cell genesis in the hippocampus and surrounding areas of the primate brain. Bromodeoxyuridine (BrdU, a marker of cell proliferation) will be injected into both young and old rhesus monkeys (Macaca mulatta). After injection of BrdU, a subset of monkeys will be given a behavioral task to induce neurogenesis. Post-mortem analysis of brain tissue using immunohistochemistry, stereology, and confocal microscopy, will identify newly created neurons, astrocytes, and oligodendrocytes. This study will analyze two sets of experimental data. 1) Differentiation of newly created cells under basal conditions will be examined in young and old animals. Preliminary results suggest that there are changes in adult cell genesis with age; the details of these changes will be explored. 2) Learning has been shown to increase adult neurogenesis in the hippocampus. This plasticity will be compared in young and old animals that received post-BrdU behavioral testing. It has been established that cognitive decline occurs with age. This proposed investigation will determine if there are changes in adult cell genesis that could be important in the neurobiological basis of age-related cognitive decline. [unreadable] [unreadable]
|
0.915 |
2019 — 2021 |
Ngwenya, Laura Benjamin |
K08Activity Code Description: To provide the opportunity for promising medical scientists with demonstrated aptitude to develop into independent investigators, or for faculty members to pursue research aspects of categorical areas applicable to the awarding unit, and aid in filling the academic faculty gap in these shortage areas within health profession's institutions of the country. |
Spreading Depolarizations and Brain Dysfunction Following Traumatic Brain Injury @ University of Cincinnati
Project Summary Traumatic brain injury (TBI) affects 2.8 million people in the US annually, but despite the heightened awareness and community interest in TBI, there are no effective interventions for TBI associated morbidities, especially cognitive impairment. Interestingly, more than 50% of patients with TBI show cortical spreading depolarizations (SDs) during their hospitalization. These ?brain tsunamis? are a predictor of mortality and morbidity after injury. Despite the fact that SDs occur often after TBI, the combined impact of SDs and TBI is unknown. The present study will determine the impact of SDs on TBI-induced pathology, providing critical guidance for targeted therapeutic intervention. Our overall hypothesis is that the occurrence of spreading depolarizations after TBI exacerbates brain pathology and is especially disruptive of hippocampal function. We will test this by inducing SDs in a rat model of TBI and addressing three specific aims. In Aim 1 we will investigate whether TBI+SDs causes greater injury pathology and aberrant neurogenesis. In Aim 2 we will determine whether SDs lead to deficits in hippocampal dependent behaviors and epilepsy. In our exploratory Aim 3 we will conduct single cell RNA sequencing on hippocampal dentate gyrus cells to identify cell-type specific molecular disturbances to guide future studies. The proposal will allow Dr. Ngwenya to learn new experimental and analytic techniques that will aid in her development as an independent researcher and position her to ask and answer the largest possible questions in translational neuroscience.
|
0.961 |