DONNA L. MCPHIE, PHD
- Harvard title(s): Instructor in Psychiatry, Harvard Medical School
- Email: email@example.com
- Telephone: (617) 855-3643
- Fax: (617) 855-3793
- Office Address: Molecular Neurogenetics Laboratory
- Degree(s): Donna McPhie received her Ph.D. in Physiology and Biophysics with a specialization in Neuroscience from Georgetown University in 1994.
- Clinical Interests: Dr. McPhie is an Instructor in the Laboratory of Molecular Neurogenetics. Her work focuses APP (Amyloid Precursor Protein) as a signaling molecule. By understanding the nature of APP's normal cellular function we can then use this information to observe and comprehend the role of perturbed signal transduction pathways in Alzheimer's Disease. Our ultimate goal is to determine points of therapeutic intervention within these signal transduction systems.
- Ito E, Oka K, Etcheberrigaray R, Nelson TJ, McPhie DL, Tofel-Grehl B, Gibson GE, Alkon DL. Internal Ca2+ mobilization is altered in fibroblasts from paitents with Alzheimer's Disease. PNAS 1994; 91: 534-538.
- Oster-Granite ML, McPhie DL, Greenan J, Neve RL. Age-dependent neuronal and synaptic degeneration in mice transgenic for the C terminus of the amyloid precursor protein. J Neurosci 1996; 16:6723-6741.
- 3. Nelson TJ, Cavallaro S, Yi C, McPhie D, Schreurs BG, Gusev PA, Favit A, Zohar O, Kim J, Beushausen S, Ascoli G, Olds J, Neve R, Alkon DL. Calexcitin: A signaling protein that binds calcium and GTP, inhibits potassium channels, and enhances membrane excitibility. PNAS 1996; 93:13808-13813
- Neve RL, Boyce FM, McPhie DL,
Greenan J, Oster-Granite ML. Transgenic mice expressing
APP-C100 in the brain. Neurobiology of Aging. 1996; 17:191-203.
- McPhie DL, Lee RKK, Eckman CD,
Olstein DL, Durham SP, Yager D, Younkin SG, Wurtman
RJ, Neve RL. Neuronal expression of b-amyloid precursor
protein Alzheimer mutations cause intracellular
accumulation of a c-termainal fragment containing
both Amyloid b and cytoplasmic domains. JBC 1997;
- Bursztajn S, DeSouza R, McPhie DL, Berman SA, Shioi J, Robakis NK, Neve R.L. Overexpression in neurons of human presenilin-1 or a presenilin-1 familial Alzheimer disease mutant does not enhance apoptosis. J. Neurosci . 1998;18:9790-9799
- Neve RL, Coopersmith R, McPhie DL, Santeufemio C, Pratt KG, Murphy CJ, Lynn SD. The Neuronal growth associated protein GAP-43 interacts with Rabaptin-5 and participates in endocytosis. J. Neurosci 1998; 18: 7757-7767.
- Berger-Sweeney J, McPhie DL,
Arters JA, Greenan J, Oster-Granite ML, Neve RL.
Impairment in spatial learning accompanied by neurodegeneration
in mice transgenic for the carboxyl-terminus of
the amyloid precursor protein, Mol Brain Res 1999;
- Pascale A, Bhagavan S, Neve RL,
McPhie DL, Etcheberrigaray R. Enhanced BK-induced
calcium responsiveness in PC12 cells expressing
the C100 fragment of the amyloid precursor protein.
Brain Res Mol Brain Res 1999; 72:205-213.
- Chen Y, McPhie DL, Hirschberg J, Neve RL. The amyloid precursor protein-binding protein APP-BP1 drives the cell cycle through the S-M checkpoint and causes apoptosis in neurons. J Biol Chem 2000. 275:8929-35.
- Neve RL, McPhie DL, Chen Y. Alzheimer's disease: a dysfunction of the amyloid precursor protein. Brain Research 2000, 886: 54-66.
- Carlezon WA, Todtenkopf MS, McPhie DL, Pimentel P, Pliakas AM, Stellar JR, Trzcinska M. Repeated exposure to rewarding brain stimulation downregulates GluR1 expression in the ventral tegmental area. Neuropsychopharmacology 2001. 25: 234-241.
- Querfurth HW, Suhara T, Rosen K, McPhie DL, Fujio Y, Tejada G, Neve RL, Adelman L, Walsh K. Beta-Amyloid peptide expression is sufficient for myotube death: Implications for human inclusion body myopathy. Mol.Cell.Neurosci 2001. 17:793-810.
- McPhie DL, Golde T,Eckman CB, Yager D, Younkin SG, Neve RL. The beta-secretase cleavage product of the amyloid precursor protein mediates neuronal apoptosis caused by familial Alzheimer's disease mutations. Mol Brain Res, 2001, 97:103-113
- Chen Y, Liu W, McPhie DL, Hassinger L, Neve RL. APP-BP1 mediates APP-induced apoptosis and DNA synthesis and is increased in Alzheimer's disease brain. J Cell Biol 2003; 163:27-33.
- McPhie DL, Coopersmith R, Hines-Peralta A, Chen Y, Ivins KJ, Manly SP, Kozlowski MR, Neve KA, Neve RL. DNA synthesis and neuronal apoptosis caused by familial Alzheimer disease mutants of the amyloid precursor protein are mediated by the p21 activated kinase PAK3. J Neurosci 2003; 23:6914-6927.