Area:
Drosophila, excitatory transmission, inhibitory transmission
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High-probability grants
According to our matching algorithm, Daewoo Lee is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2005 — 2006 |
Lee, Daewoo |
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.) |
Role of Dopamine in Alpha-Syn-Mediated Neurodegeneration
DESCRIPTION (provided by applicant): Since the synapse is a functional building block of the brain, defects in, or loss of, specific synaptic signaling/modulation consequently underlies neurological disorders such as Parkinson's disease (PD). Therefore, our interests are to understand the cellular and molecular mechanisms underlying selective degeneration of dopaminergic (DA) neurons and synapses. Among the proposed underlying causes of DA cell death, oxidative damage is thought to play an important role. Ironically, neurotransmitter dopamine itself can become a source of oxidative stress and consequently contribute to the selective DA cell death in PD. This study aims to reveal mechanisms underlying dopamine's ability to mediate alpha-synuclein-induced neurodegeneration. We will employ molecular genetic, immunocytochemical and amperometrical approaches applied to a variety of transgenic fly lines and primary neuronal cultures as a model system. The results of our experiments will contribute to our understanding of the molecular mechanisms of how alpha-synuclein induces disruption of DA homeostasis, resulting in elevated levels of cytoplasmic DA and eventually leading to specific neuronal death. The high degree of conservation between vertebrates and invertebrates in terms of the basic mechanisms important in DA modulation, suggests that our studies in Drosophila will be important in guiding development of rational treatment strategies aimed at restoring dopamine function/homeostasis that has been disrupted in Parkinson's disease patients. In addition, amperometric recordings of synaptic DA release and cytoplasmic DA concentrations will be very useful not only to characterize the relationship between DA homeostasis and specific neurodegeneration, but also to study DA signaling mechanisms mediating learning/memory and drug addiction.
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1 |
2020 |
Lee, Daewoo |
R15Activity Code Description: Supports small-scale research projects at educational institutions that provide baccalaureate or advanced degrees for a significant number of the Nation’s research scientists but that have not been major recipients of NIH support. The goals of the program are to (1) support meritorious research, (2) expose students to research, and (3) strengthen the research environment of the institution. Awards provide limited Direct Costs, plus applicable F&A costs, for periods not to exceed 36 months. This activity code uses multi-year funding authority; however, OER approval is NOT needed prior to an IC using this activity code. |
Phosphorylation-Dependent Human Tau Release
Neurofibrillary tangles (NFT) are a hallmark of Alzheimer's disease (AD) and related dementias. NFTs are of growing biomedical interest as the temporal and spatial pattern of NFT appearance in human brain correlates well with AD progression. The tangle is composed of microtubule associated protein tau, which can be hyper-phosphorylated and aggregated. Indeed, tau protein purified from the brains of AD patients is hyper-phosphorylated, which has led to investigations of the role of tau phosphorylation in mediating neurodegeneration. Alzheimer's pathogenic mechanisms still remain elusive. Recently, an intriguing concept of prion-like spreading of tau has emerged, which has the potential to transform AD research. A prion-like mechanism involving the transfer of hyper-phosphorylated tau between synaptically connected neurons underlies the seeding and spread of tau pathology. New insights into the molecular mechanisms of tau propagation will uncover potential therapeutic targets for slowing or even halting AD progression. Hyper-phosphorylation of tau is also known to be involved in tau release, causing its cell-to-cell propagation. However, there is still a significant gap in understanding how phosphorylation regulates tau release. We hypothesize that individual phosphorylation sites will differentially affect tau release and that studying this phenomena will uncover a currently unexplored network of endogenous protein kinases that act to regulate tau release by phosphorylating specific residues on tau. In particular, it is not known what phosphorylation sites of tau (pTau) are crucial for its release and kinases have yet to be identified for their role in tau release - a recognized seminal step in the prion-like spreading of tau protein. In Aim 1, we will study the role of specific phosphorylation sites of tau on its release. pTau sites to be examined will be primarily in proline-rich domain (PRD) and C-terminal region of tau as ~75% of disease associated pTau sites are found in these regions. In Aim 2, we will examine 5 kinases for their role in tau release as they are known to phosphorylate amino acids in PRD and C-terminal regions. Aim 3 will test if activity-driven endogenous hTau release is modulated by phosphorylation of tau at specific amino acids using a human neural cell line (ReNCell) endogenously expressing hTau. Our approach with Drosophila (Aims 1 & 2) and human neuronal culture models (Aim 3) will also provide excellent opportunities for training and mentoring both undergraduate and graduate students.
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1 |