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High-probability grants
According to our matching algorithm, Jason D. Ulrich is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2007 — 2009 |
Ulrich, Jason D |
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.). |
Pyk2 Regulation of Nr2b Surface Expression and Tyr1472 Phosphorylation
[unreadable] DESCRIPTION (provided by applicant): NMDA receptors are critical mediators of long lasting changes in the efficacy of synaptic transmission (i.e. LTP and LTD). NMDA receptors are glutamate gated ion channels consisting of a dimer of NR1 subunits and hompdimer or heterodimer of NR2 subunits. One type of NR2 subunit, NR2B, is of particular interest due to its involvement in both synaptic plasticity and numerous neurological pathologies. NMDA receptors are upregulated by Src family kinase mediated tyrosine phosphorylation of NR2A and NR2B. One tyrosine residue of particular interest on NR2B is Tyr1472. Phosphorylation of Tyr1472 is believed to promote surface expression of NR2B containing NMDA receptors by blocking an association between NR2B and the clathrin adaptor protein AP-2. Increases in Tyr1472 phosphorylation are evident in status epilepticus, neuropathic pain, and following transient ischemia. Decreases in Tyr1472 phosphorylation have been observed in Alzheimer's disease. Src family kinases are activated in the post-synaptic density following activation of Pyk2. Pyk2 activation is dependent upon increases in intracellular Ca2+ and PKC activation. Pyk2's importance in synaptic function is underscored by the fact that Pyk2 is necessary for LTP in hippocampal neurons, and the observation that Pyk2 is upregulated following transient ischemia. We hypothesize Pyk2 is an important regulator of surface expression for NR2B containing NMDA receptors via activation of Src and/or Fyn. We propose to test our hypothesis by activating or inhibiting Pyk2 and assaying for changes in NR2B surface expression and Tyr1472 phosphorylation. In addition we will specifically inhibit Src or Fyn while activating Pyk2 and assay for changes in NR2B surface expression and Tyr1472 phosphorylation. Our results will demonstrate whether Pyk2 is important for regulating NR2B surface expression, thus making Pyk2 a potential therapeutic target in neurological disease. [unreadable] [unreadable] [unreadable]
|
0.957 |
2013 — 2014 |
Ulrich, Jason |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Co-Regulation of Apoe and Abeta by Synaptic Activity
DESCRIPTION (provided by applicant): Alzheimer's disease (AD) is the most common cause of dementia in the elderly, afflicts 1 in 8 elderly Americans, and care for AD patients incurs diret costs of approximately $200 billion annually. There is currently no effective therapy to delay AD onset or slow AD progression. Therefore, it is of critical importance to develop a better understanding of AD pathogenesis in order to develop new targets for therapeutic intervention. AD is characterized by the deposition of aggregated forms of amyloid (A?) plaques within the brain, which is hypothesized to be a critical instigator of synaptic loss and neurodegeneration. The strongest genetic determinant for the development of the most common form of AD, late onset AD, is possession of the apolipoprotein E 4 allele (APOE4). ApoE is a critical lipid transport protein in the CNS where it is expressed mainly by astrocytes. There are three common apoE variants (apoE2, apoE3, and apoE4) which differentially regulate A? clearance from the CNS and A? plaque formation. Little is known about the physiological regulation of apoE within the CNS, particularly in regard to the regulation of the levels and lipidation of the extracellular pool of apoE. We recently developed a method to measure the level and lipidation state of apoE directly from the brain parenchyma interstitial fluid (ISF) using in vivo microdialysis. Since neurons rely upon apoE to supply lipids and cholesterol to support neuronal function, we decided to test whether synaptic activity modulated apoE within the brain. Our preliminary data indicate that increasing synaptic activity increases the ISF level of apoE. Interestingly, synaptic activity has previously been shown to regulate A? production and A? ISF level. Therefore, we propose use in vivo microdialysis to investigate whether synaptic activity co-regulates apoE and A? within the ISF, and whether synaptic activity-dependent regulation of apoE level and lipidation impacts fluctuations in A? levels during physiological changes in neuronal activity, such as during the sleep- wake cycle. The results of our experiments will further our understanding of apoE regulation within the CNS and could provide insight for the development of novel AD therapies to reduce the burden of neurological disease.
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0.915 |