In Situ Neuronal Model of Phf/Tau Accumulation in Ad

Hall, Garth F.

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Institute on Aging (NIA)
• Type: Research Project (R01)
• Project #: 7R01AG013919-02
• Application #: 2442333
• Study Section: Neurological Sciences Subcommittee 1 (NLS)
• Project Start: 1996-08-15
• Project End: 2000-11-30
• Budget Start: 1997-09-15
• Budget End: 1997-11-30
• Support Year: 2
• Fiscal Year: 1996

Institution

• Name: University of Massachusetts Lowell
• Department: Biology
• Type: Schools of Arts and Sciences
• DUNS #: 956072490
• City: Lowell
• State: MA
• Country: United States
• Zip Code: 01854

Publications

Kim, Wonhee; Lee, Sangmook; Jung, Cheolwha et al. (2010) Interneuronal transfer of human tau between Lamprey central neurons in situ. J Alzheimers Dis 19:647-64

Lee, Sangmook; Jung, Cheolwha; Lee, Gloria et al. (2009) Exonic point mutations of human tau enhance its toxicity and cause characteristic changes in neuronal morphology, tau distribution and tau phosphorylation in the lamprey cellular model of tauopathy. J Alzheimers Dis 16:99-111

Hall, Garth F; Lee, Sangmook; Yao, Jun (2002) Neurofibrillary degeneration can be arrested in an in vivo cellular model of human tauopathy by application of a compound which inhibits tau filament formation in vitro. J Mol Neurosci 19:253-60

Hall, G F; Chu, B; Lee, G et al. (2000) Human tau filaments induce microtubule and synapse loss in an in vivo model of neurofibrillary degenerative disease. J Cell Sci 113 ( Pt 8):1373-87

Hall, G F; Chu, B; Lee, S et al. (2000) The single neurofilament subunit of the lamprey forms filaments and regulates axonal caliber and neuronal size in vivo. Cell Motil Cytoskeleton 46:166-82

Hall, G F; Yao, J; Lee, G (1997) Human tau becomes phosphorylated and forms filamentous deposits when overexpressed in lamprey central neurons in situ. Proc Natl Acad Sci U S A 94:4733-8