Area:
Drosophila nervous system development
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High-probability grants
According to our matching algorithm, Brian D. McCabe is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2010 — 2014 |
Mccabe, Brian D |
P50Activity Code Description: To support any part of the full range of research and development from very basic to clinical; may involve ancillary supportive activities such as protracted patient care necessary to the primary research or R&D effort. The spectrum of activities comprises a multidisciplinary attack on a specific disease entity or biomedical problem area. These grants differ from program project grants in that they are usually developed in response to an announcement of the programmatic needs of an Institute or Division and subsequently receive continuous attention from its staff. Centers may also serve as regional or national resources for special research purposes. |
Retromer Trafficking and Alzheimer's Disease in Drosophila @ Columbia University Health Sciences
Late-Onset Alzheimer's disease (LOAD) is biochemically characterized by abnormal elevations of AB peptide and increased tau phosphorylation. Recently, reduced activity ofthe Retromer complex, which is important for the recycling of transmembrane receptors from endosomes to the Trans-Golgi Network (TGN), has been implicated in the pathology of LOAD from human patient expression profiling. The importance of retromer trafficking to LOAD is supported by several studies including both mouse and Drosophila genetic models of retromer deficiency, which have increased levels of Ap peptide, neurological deficits, and in the fly, extensive neurodegeneration. Defective retromer trafficking also inhibits Wnt signaling, suggesting a pathway via glycogen synthase kinase 3 beta (GSKSp) through which retromer could alter tau phosphorylation. We hypothesize that defective retromer sorting is central to both elevated AB peptide levels and increased tau phosphorylation in LOAD and that modulating retromer trafficking levels will have a positive impact on neurodegeneration. We will test this hypothesis in transgenic Drosophila models of LOAD where human Amyloid Precursor Protein (APP) and Amyloid Precursor Protein li-secretase (BACE) or human Tau are expressed. Our specific aims are designed to determine the molecular pathway that connects retromer deficiency to neurodegeneration and characterize novel interacting proteins that could promote retromer stability.
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1 |
2011 — 2012 |
Mccabe, Brian D |
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.) |
Deciphering the Genetics of Synapse Development by Whole Genome Sequencing @ Columbia University Health Sciences
DESCRIPTION (provided by applicant): Screening for mutants that disrupt neurodevelopmental processes in model systems such as Drosophila and the subsequent identification of the causative molecules have been central to understanding of the genetic basis of nervous system development. However, the full promise of forward genetic screening to discern the total complement of genes required for a neurobiological process is rarely realized, in part due to the time and labor required to identify the disrupted genes through conventional genetic mapping techniques. Recent years have seen proof-of-principle studies on the use of Whole Genome Sequencing (WGS) to identify causative point mutations in chemically mutagenized C.elegans or Drosophila strains. In both cases, the strategy was fast and cost-effective. We propose to recruit WGS technology to identify the molecular lesions in a large collection of Drosophila neuromuscular junction (NMJ) synapse mutants we have generated in preliminary studies. Using conventional genetic mapping techniques, we have previously identified the disrupted genes in subset of these mutants and subsequently characterized both novel synaptic regulatory pathways as well mutations in the Drosophila orthologs of human disease relevant proteins. We will determine the causative genetic defect in an additional forty selected synaptic structure mutants with the goal to both increase our understanding of the molecular regulation of synapse development and provide a guide for future, in-depth analysis of the uncovered loci. Furthermore, the repeated, routine application of Whole Genome Sequencing will supply valuable information on the reproducibility and reliability of this approach and establish the technology as a state-of-the-art cloning technique for nervous system mutants in Drosophila and other neurogenetic model systems. PUBLIC HEALTH RELEVANCE: We will conscript the most current high throughput whole genome sequencing and cloning technology and apply it to neurodevelopment mutants. Establishment of this technology as a state-of-the-art method to identify genes that regulate neurodevelopment will rapidly expand the compendium of molecules associated with normal and aberrant nervous system development, many of which are likely to play important roles in human neurological disease.
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