The Core has developed within the Mailman Research Center as an outgrowth of our Effect: Molecular Biology of Neuronal . The Program allowed sections of Dr. Marottals laboratory that are directed by Dr. Majocha to be joined with Dr. Benes' neuroanatomy facility. The combined resource spans the major divisions of the Center and has established fruitful collaborations with many investigators of the Program. Establishment of a proposed formal core avoids duplication of efforts, techniques and equipment, and the Core is expected to foster more efficient collaborative interactions among the participants in the Program. The member of the Core will provide qualitative and quantitative cytochemical and histological services at the light and electron microscopic levels in order to facilitate the studies of the various Projects. The core is able to provide the following: a fixed postmortem control and AD brain tissues; b. common and specialized staining techniques; c. preparation, characterization and application of polyclonal and monoclonal antibodies; d. in situ hybridization methodology; e. quantitative and qualitative light and electron microscopic analyses of specimens; f. data analysis.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Program Projects (P01)
Project #
5P01AG002126-11
Application #
3802340
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
11
Fiscal Year
1991
Total Cost
Indirect Cost
Name
Mc Lean Hospital (Belmont, MA)
Department
Type
DUNS #
City
Belmont
State
MA
Country
United States
Zip Code
02478
Li, J; Hertzberg, E L; Nagy, J I (1997) Connexin32 in oligodendrocytes and association with myelinated fibers in mouse and rat brain. J Comp Neurol 379:571-91
Nagy, J I; Hossain, M Z; Hertzberg, E L et al. (1996) Induction of connexin43 and gap junctional communication in PC12 cells overexpressing the carboxy terminal region of amyloid precursor protein. J Neurosci Res 44:124-32
Sandhu, F A; Kim, Y; Lapan, K A et al. (1996) Expression of the C terminus of the amyloid precursor protein alters growth factor responsiveness in stably transfected PC12 cells. Proc Natl Acad Sci U S A 93:2180-5
Nagy, J I; Li, W; Hertzberg, E L et al. (1996) Elevated connexin43 immunoreactivity at sites of amyloid plaques in Alzheimer's disease. Brain Res 717:173-8
Lynn, B D; Marotta, C A; Nagy, J I (1995) Propagation of intercellular calcium waves in PC12 cells overexpressing a carboxy-terminal fragment of amyloid precursor protein. Neurosci Lett 199:21-4
Friedland, R P; Majocha, R E; Reno, J M et al. (1994) Development of an anti-A beta monoclonal antibody for in vivo imaging of amyloid angiopathy in Alzheimer's disease. Mol Neurobiol 9:107-13
Maestre, G E; Tate, B A; Majocha, R E et al. (1994) Intercellular interactions in PC12 cells overexpressing beta/A4 amyloid. Scanning Microsc 8:325-35;discussion 335-6
Majocha, R E; Agrawal, S; Tang, J Y et al. (1994) Modulation of the PC12 cell response to nerve growth factor by antisense oligonucleotide to amyloid precursor protein. Cell Mol Neurobiol 14:425-37
Leli, U; Shea, T B; Cataldo, A et al. (1993) Differential expression and subcellular localization of protein kinase C alpha, beta, gamma, delta, and epsilon isoforms in SH-SY5Y neuroblastoma cells: modifications during differentiation. J Neurochem 60:289-98
Majocha, R E; Tate, B; Marotta, C A (1993) PC12 cells release stimulatory factors after transfection with beta/A4-C-terminal DNA of the Alzheimer amyloid precursor protein. Mol Chem Neuropathol 18:99-113

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