Neuroscience 2000 Abstract
| Presentation Number: | 380.14 |
|---|---|
| Abstract Title: | Postmortem levels of p25 and CDK5 in brains with Alzheimer's disease and other neurodegenerative disorders. |
| Authors: |
Tandon, A.*1
; Yu, H.1
; Rogaeva, E.1
; Sato, C.1
; Kawarai, T.1
; St George-Hyslop, P.1
1Ctr Res Neurodegenerative Diseases, Univ Toronto, Toronto, Canada |
| Primary Theme and Topics |
J. Disorders of the Nervous System and Aging - 130. Degenerative disease: Alzheimer's-other |
| Secondary Theme and Topics | B. Cell Biology<br />- 27. Membrane structure and cytoskeleton |
| Session: |
380. Degenerative disease: Alzheimer's--other: tau II Poster |
| Presentation Time: | Monday, November 6, 2000 2:00 PM-3:00 PM |
| Location: | Hall G-J |
| Keywords: | tau, human brain, neurodegeneration, neurofibrillary tangles |
Alzheimer's disease (AD) is most common neurodegenerative disorder associated with aging, manifest as progressive dementia with extensive cortical atrophy, extracellular amyloid deposits that contain Aβ peptide, and intracellular neurofibrillary tangles (NFT) composed of hyperphosphorylated tau. While much progress has been made in clarifying the biology of the Aβ peptide, the regulation of tau processing is less well understood. A recent report suggested that NFT in AD might result from increased activation of CDK5-mediated phosphorylation of tau, a consequence of constitutive activation of the kinase by its regulatory component p25. The present study examines the levels of p25, its precursor p35, and CDK5 in brains of patients with AD, familial AD (FAD), and other neurodegenerative disorders which display NFT such as Down's syndrome (DS), Parkinson's disease (PD), Pick's disease, corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), and frontotemporal dementia (FTD). While CDK5 levels were similar between control and diseased brains, the amount of p25, detected by the a polyclonal antibody raised to the C-terminal portion of p35 (C-19; Santa Cruz), exhibited wide variation. Six of eight control brains, which displayed no detectable NFT on postmortem examination, had elevated levels of p25, relative to the AD brains (n=5), but similar to that of FAD brains (n=2). Moreover, intermediate levels of p25 immunoreactivity were detected in DS, PD, CBD and PSP (n=2, each). Our results suggest that an increase in p25 immunoreactivity alone cannot account for the increased tau phosphorylation in AD brains.
Supported by MRC of Canada
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2000 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2000. Online.
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