Neuroscience 2002 Abstract
| Presentation Number: | 592.9 |
|---|---|
| Abstract Title: | ATYPICAL PROTEIN KINASE C (PKC) COLOCALIZES WITH TAU- AND α-SYNUCLEIN-RELATED INCLUSIONS IN NEURODEGENERATIVE DISORDERS. |
| Authors: |
Shao, C. Y.*1
; Crary, J. F.2
; Sheffied, L. G.1
; Braithwaite-Harte, L.1
; Hernandez, I.2
; Tcherepanov, A.2
; Sacktor, T. C.2,3
; Mirra, S. S.1
1Pathology, SUNY Downstate Medical Center, Brooklyn, NY 2Physiology/Pharmacology, SUNY Downstate Medical Center, Brooklyn, NY 3Neurology, SUNY Downstate Medical Center, Brooklyn, NY |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neurodegenerative Disorders -- Alzheimers Disease: Tau |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Neurodegenerative Disorders<br />-- Alzheimers Disease: Other |
| Session: |
592. Neurodegenerative disorders: Alzheimer's disease--tau III Poster |
| Presentation Time: | Tuesday, November 5, 2002 1:00 PM-2:00 PM |
| Location: | Hall A2-B3 W-15 |
| Keywords: | Alzheimer's disease, Pick's disease, Lewy body, corticobasal degeneration |
Tau-associated filamentous aggregates are neuropathological hallmarks of Alzheimer’s disease (AD), Pick's disease (PiD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD), whereas α-synuclein-positive Lewy bodies are features of Parkinson’s disease (PD) and dementia with Lewy bodies (DLB). Factors underlying the genesis and functional impact of these aggregates remain poorly understood. Protein kinase M zeta (PKMζ), the catalytic fragment of PKCζ, plays a key role in the maintenance of long-term potentiation, a widely studied model of memory and synaptic plasticity (Ling et al. Nat Neurosci 5:295, 2002). We have demonstrated an association of PKMζ and atypical PKCs (ι and ζ) with neurofibrillary tangles and Hirano bodies in AD (Crary et al. Soc Neurosci Abs, 2002). In the present study, we investigated the relationship of atypical PKCs and PKMζ to abnormal inclusions in PiD (n=2); PSP (n=3); CBD (n=3); and DLB with AD (n=3). Immunohistochemical study was performed on autopsy brain tissue using antibodies targeting epitopes of the two known isoforms of atypical PKC (PKMζ and ι/λ). Preliminary results reveal that these antibodies label with varying intensity a subset of neuronal and glial inclusions in CBD, Pick bodies and Hirano bodies in PiD, globose neurofibrillary tangles in PSP, and Lewy bodies in DLB. The association of PKMζ and atypical PKCs with tau, α-synuclein, and actin-related filamentous aggregates suggests that these kinases may play a role in the pathogenesis of these neurodegenerative disorders.
Supported by K07 AG00959
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
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