The overall goal of this interinstitutional NINDS P30 Core Grant is to foster new interdisciplinary collaborations among neuroscientists in La Jolla institutions by allowing access to scientific cores to which they were previously denied or had little access, and by promoting new cores to promote state-of-the-art technology;these cores were started under the prior auspices of the NIH Blueprint Core Grant (P30 NS057096) that was awarded to the PI, Dr. Lipton, for the past five years. Since the entire Blueprint Core Grant Program has been terminated by NIH, NINDS Program Officials asked us to submit this NINDS P30 Core Grant. To accomplish our goal, we have chosen among the very best core facilities on the Blueprint Core Grant, and have chosen top scientists to run these cores at the Sanford-Burnham Medical Research Institute (SBMIR) and the University of California San Diego (UCSD) in order to assist NINDS neuroscientists in La Jolla. The cores proposed here represent (i) High-Throughput (HS) Library Screening (at SBMRI), (ii) Neuropathology (at UCSD), and (iii) Electrophysiology (at SBMIR with Advisors at Salk), in addition to (iv) an Administrative Core (centered at SBMRI). These Core Facilities will be available to neuroscientists at all four institutions on the La Jolla Torrey Pines Mesa, composed of SBMRI, UCSD, Salk, and The Scripps Research Institute. These institutions share one of the top-rated neuroscience graduate programs in the country and have committed considerable institutional funds towards these cores. This work is aimed at developing new treatments for neurological disorders.
The Specific Aims, which will be facilitated by all 3 Scientific Cores and the Administrative Core, are as follows: 1. To obtain Core support for Neuroscientists studying Neurodegenerative Disorders. The Cores will also help develop Neuroprotective Therapies. These disorders, represented in the Qualifying NINDS Projects of Major USERS, include Alzheimer's, Parkinson's, ALS, and Huntington's disease. 2. To obtain Core support for Neuroscientists studying Neoplastic Disorders of the brain. These disorders, represented in the Qualifying NINDS Projects of Major USERs, include glioblastoma multiforme and medulloblastoma tumors. 3. To obtain Core support for Neuroscientists studying Developmental Disorders. Disorders include abnormal neuronal migration, and are represented in NINDS Qualifying Projects of Major USERs.
This NINDS Neuroscience P30 Core Grant will provide facilities to enable neuroscientists in La Jolla to pursue their work on novel therapies for Neurodegenerative Disorders, Neoplastic Disorders of the Brain (tumors), and Neurodevelopmental Disorders.
|Mann, Aman P; Scodeller, Pablo; Hussain, Sazid et al. (2018) Publisher Correction: Identification of a peptide recognizing cerebrovascular changes in mouse models of Alzheimer's disease. Nat Commun 9:1070|
|Ryan, Tammy; Bamm, Vladimir V; Stykel, Morgan G et al. (2018) Cardiolipin exposure on the outer mitochondrial membrane modulates ?-synuclein. Nat Commun 9:817|
|Nagar, Saumya; Noveral, Sarah M; Trudler, Dorit et al. (2017) MEF2D haploinsufficiency downregulates the NRF2 pathway and renders photoreceptors susceptible to light-induced oxidative stress. Proc Natl Acad Sci U S A 114:E4048-E4056|
|Huang, Timothy Y; Zhao, Yingjun; Jiang, Lu-Lin et al. (2017) SORLA attenuates EphA4 signaling and amyloid ?-induced neurodegeneration. J Exp Med 214:3669-3685|
|Mann, Aman P; Scodeller, Pablo; Hussain, Sazid et al. (2017) Identification of a peptide recognizing cerebrovascular changes in mouse models of Alzheimer's disease. Nat Commun 8:1403|
|Tu, Shichun; Akhtar, Mohd Waseem; Escorihuela, Rosa Maria et al. (2017) NitroSynapsin therapy for a mouse MEF2C haploinsufficiency model of human autism. Nat Commun 8:1488|
|Oh, Chang-Ki; Sultan, Abdullah; Platzer, Joseph et al. (2017) S-Nitrosylation of PINK1 Attenuates PINK1/Parkin-Dependent Mitophagy in hiPSC-Based Parkinson's Disease Models. Cell Rep 21:2171-2182|
|Satoh, Takumi; Lipton, Stuart (2017) Recent advances in understanding NRF2 as a druggable target: development of pro-electrophilic and non-covalent NRF2 activators to overcome systemic side effects of electrophilic drugs like dimethyl fumarate. F1000Res 6:2138|
|Nakamura, Tomohiro; Lipton, Stuart A (2017) 'SNO'-Storms Compromise Protein Activity and Mitochondrial Metabolism in Neurodegenerative Disorders. Trends Endocrinol Metab 28:879-892|
|Chen, Shanyan; Cui, Jiankun; Jiang, Tao et al. (2017) Gelatinase activity imaged by activatable cell-penetrating peptides in cell-based and in vivo models of stroke. J Cereb Blood Flow Metab 37:188-200|
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