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High-probability grants
According to our matching algorithm, Larry S. Sherman is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2019 — 2020 |
Sherman, Larry S |
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.) |
Hyaluron as a Regulator of Chemotherapy-Induced Changes in Neurogenesis @ Oregon Health & Science University
Post-chemotherapy induced cognitive impairment, also called ?chemobrain,? affects large numbers of cancer patients and survivors, and is characterized by subjectively reported and objectively measured cognitive deficits following cancer chemotherapy. These deficits can last for up to several years and significantly impact the quality of life of affected patients. Recent findings have indicated that declines in neurogenesis, particularly by neural stem cells (NSCs) in the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG), contribute to cognitive dysfunction following treatment with a number of different chemotherapy agents. Our preliminary data indicate that the glycosaminoglycan hyaluronan (HA) is reduced in the dentate gyri of mice treated with a common chemotherapy agent, 5-fluorouracil (5-FU). Disruption of HA in the SGZ leads to increased NSC proliferation and increased numbers of neuronal progenitors whose maturation is delayed in the granule cell layer of the dentate gyrus. Similarly, mice lacking the major transmembrane HA receptor CD44 demonstrate increased NSC proliferation in the SGZ and delayed neuronal progenitor cell maturation in the dentate gyrus. These mice also demonstrate cognitive deficits related to altered hippocampal function. These data support the novel hypothesis that chemotherapy can alter the HA-based hippocampal extracelluar matrix either by increasing hyaluronidase activity or decreasing HA synthesis, leading to the disruption of HA in the SGZ. This disruption would initially lead to increased NSC proliferation and delayed or aberrant neuronal differentiation, and the eventual exhaustion of NSCs and reduced neurogenesis. Our aim in the current application is to test this hypothesis in a rodent model of chemotherapy with the long-term goal of developing strategies that can enhance or protect neurogenesis during cancer therapies. Our specific aims are: (1) To test the hypothesis that chemotherapy leads to the induction of hyaluronidases and the accumulation of specific HA digestion products in the hippocampus; and (2) To test the hypothesis that chemotherapy-induced HA digestion leads to aberrant adult neurogenesis. All together, these studies have the potential to reveal a novel mechanism by which hippocampal neurogenesis is disrupted in individuals with chemobrain and will begin to test the efficacy of interfering with hyaluronidase activity as a means of enhancing neurogenesis in cancer patients undergoing chemotherapy.
|
0.915 |
2020 |
Sherman, Larry S |
R24Activity Code Description: Undocumented code - click on the grant title for more information. |
A Non-Human Primate Resource For Pre-Clinical Studies of Neurodegenerative Disease @ Oregon Health & Science University
This application aims to develop a highly novel non-human primate (NHP) resource for investigators performing pre-clinical studies in three neurodegenerative diseases that affect humans: multiple sclerosis (MS), Batten disease, and age-related macular degeneration (AMD). Subpopulations of Japanese macaques (JMs) housed at the Oregon National Primate Research Center (ONPRC) spontaneously develop conditions that mimic each of these diseases. Japanese macaque encephalomyelitis (JME) shares many of the pathophysiological features of multiple sclerosis (MS) in humans including demyelination and axonal damage linked to nervous system attacks by myelin-reactive immune cells. Japanese macaque Batten disease (JMBD) is genetically and pathophysiologically similar to a form of human neuronal ceroid lipofuscinosis (CLN7) that causes vision loss, motor dysfunction and other neurological symptoms. Japanese macaque dominant drusen (JMDD) is a model of human AMD, which is the leading cause of vision loss among people over the age of 50. At present, there are limited or no treatments for any of the human forms of these diseases, making these NHP models extraordinarily valuable to the research community. Ongoing studies in each of these NHP disease models have demonstrated that specific groups of animals within the colony or animals with specific genotypes are pre-disposed to each of these conditions. As a result, it is possible to generate animals that develop each disease through targeted breeding, providing a unique opportunity to generate a resource for investigators focused on studying mechanisms of disease onset and progression, or who are developing strategies to treat each disease. We therefore aim to: (1) develop targeted breeding colonies of JME, JMBD, and JMDD animals; and (2) develop a bank of tissues from unaffected JMs and animals with JME, JMBD, and JMDD. All together, this proposal will develop a novel resource that will provide investigators interested in MS, Batten disease, or AMD with access to animals and tissues to support pre-clinical studies aimed at delaying, halting or reversing disease progression.
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0.915 |