Biology of Alzheimer Paired Helical Filaments

Lee, Virginia M.

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Institute on Aging (NIA)
• Type: Research Project (R01)
• Project #: 5R01AG010210-05
• Application #: 2051479
• Study Section: Neurological Sciences Subcommittee 1 (NLS)
• Project Start: 1992-06-15
• Project End: 1997-05-31
• Budget Start: 1996-06-01
• Budget End: 1997-05-31
• Support Year: 5
• Fiscal Year: 1996

Institution

• Name: University of Pennsylvania
• Department: Pathology
• Type: Schools of Medicine
• DUNS #: 042250712
• City: Philadelphia
• State: PA
• Country: United States
• Zip Code: 19104

Publications

D'Souza, I; Poorkaj, P; Hong, M et al. (1999) Missense and silent tau gene mutations cause frontotemporal dementia with parkinsonism-chromosome 17 type, by affecting multiple alternative RNA splicing regulatory elements. Proc Natl Acad Sci U S A 96:5598-603

Clark, L N; Poorkaj, P; Wszolek, Z et al. (1998) Pathogenic implications of mutations in the tau gene in pallido-ponto-nigral degeneration and related neurodegenerative disorders linked to chromosome 17. Proc Natl Acad Sci U S A 95:13103-7

Mills, J C; Lee, V M; Pittman, R N (1998) Activation of a PP2A-like phosphatase and dephosphorylation of tau protein characterize onset of the execution phase of apoptosis. J Cell Sci 111 ( Pt 5):625-36

Hoffmann, R; Lee, V M; Leight, S et al. (1997) Unique Alzheimer's disease paired helical filament specific epitopes involve double phosphorylation at specific sites. Biochemistry 36:8114-24

Lee, V M (1995) Disruption of the cytoskeleton in Alzheimer's disease. Curr Opin Neurobiol 5:663-8

Goedert, M; Jakes, R; Crowther, R A et al. (1993) The abnormal phosphorylation of tau protein at Ser-202 in Alzheimer disease recapitulates phosphorylation during development. Proc Natl Acad Sci U S A 90:5066-70