We propose to establish an Antibody Core at the Rockefeller University which will serve as an antibody resource for investigators participating in the ADCC. The initial focus of the Core will be to produce, store and provide antibodies relevant to the study of APP and Abeta. Much of our understanding of the processing of APP, the production of Abeta, and the formation of insoluble Abeta-amyloid has depended on experiments carried out using well-defined antibodies. Furthermore, such antibodies have also been extensively used to examine the neuropathological progression of Abeta-amyloidosis. The recent discovery of APP-related proteins which cross-react with anti-APP antibodies but are not a source of Abeta makes the development of APP-specific antibodies particularly important. We propose to prepare a large panel of monoclonal antibodies with defined properties to be used for studies of APP processing. Abeta production, and Abeta amyloidogenesis. The establishment of this Antibody Core will provide valuable support to researchers at Rockefeller, NYU, IBR and NKI who are participating in the ADCC, as well as to scientists at other ADCs. Studies using core resources will be more cost effective, and in some instances projects will be conducted that would not be feasible without the availability of these antibodies. Establishment of this Core also will strengthen the involvement of The Rockefeller University Laboratory of molecular and Cellular Neuroscience in the ADCC.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Center Core Grants (P30)
Project #
5P30AG008051-07
Application #
5204592
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
7
Fiscal Year
1996
Total Cost
Indirect Cost
Ting, Simon Kang Seng; Foo, Heidi; Chia, Pei Shi et al. (2018) Dyslexic Characteristics of Chinese-Speaking Semantic Variant of Primary Progressive Aphasia. J Neuropsychiatry Clin Neurosci 30:31-37
Ramos-Cejudo, Jaime; Wisniewski, Thomas; Marmar, Charles et al. (2018) Traumatic Brain Injury and Alzheimer's Disease: The Cerebrovascular Link. EBioMedicine 28:21-30
Jeanneteau, Freddy; Barrère, Christian; Vos, Mariska et al. (2018) The Stress-Induced Transcription Factor NR4A1 Adjusts Mitochondrial Function and Synapse Number in Prefrontal Cortex. J Neurosci 38:1335-1350
Drummond, Eleanor; Nayak, Shruti; Pires, Geoffrey et al. (2018) Isolation of Amyloid Plaques and Neurofibrillary Tangles from Archived Alzheimer's Disease Tissue Using Laser-Capture Microdissection for Downstream Proteomics. Methods Mol Biol 1723:319-334
Ramsey, Christine M; Gnjidic, Danijela; Agogo, George O et al. (2018) Longitudinal patterns of potentially inappropriate medication use following incident dementia diagnosis. Alzheimers Dement (N Y) 4:1-10
Chen, Jingyun; Li, Yi; Pirraglia, Elizabeth et al. (2018) Quantitative evaluation of tau PET tracers 18F-THK5351 and 18F-AV-1451 in Alzheimer's disease with standardized uptake value peak-alignment (SUVP) normalization. Eur J Nucl Med Mol Imaging 45:1596-1604
Hadjichrysanthou, Christoforos; McRae-McKee, Kevin; Evans, Stephanie et al. (2018) Potential Factors Associated with Cognitive Improvement of Individuals Diagnosed with Mild Cognitive Impairment or Dementia in Longitudinal Studies. J Alzheimers Dis 66:587-600
de Leon, Mony J; Li, Yi; Rusinek, Henry (2018) Reply: Cerebrospinal Fluid, Hyposmia, and Dementia in Alzheimer Disease: Insights from Dynamic PET and a Hypothesis. J Nucl Med 59:718-719
Hanfelt, John J; Peng, Limin; Goldstein, Felicia C et al. (2018) Latent classes of mild cognitive impairment are associated with clinical outcomes and neuropathology: Analysis of data from the National Alzheimer's Coordinating Center. Neurobiol Dis 117:62-71
Burke, Shanna L; Hu, Tianyan; Fava, Nicole M et al. (2018) Sex differences in the development of mild cognitive impairment and probable Alzheimer's disease as predicted by hippocampal volume or white matter hyperintensities. J Women Aging :1-25

Showing the most recent 10 out of 604 publications