Neuroscience 2001 Abstract
| Presentation Number: | 276.8 |
|---|---|
| Abstract Title: | ROLE OF CYTOSKELETAL PROTEIN, SYNAPTOPODIN IN LATE ONSET ALZHEIMER'S DISEASE PATHOGENESIS. |
| Authors: |
Reddy, P. H.*1
; Yang, R.1
; Murdoch, G.2
; Kaye, J.3
; Mani, G.1
1NSI, Oregon Health Sciences University, Beaverton, OR 2Pathology, Oregon Health Sciences University, Portland, OR 3Neurology, Oregon Health Sciences University, Portland, OR |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Cytoskeleton -- Other |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Neurodegenerative Disorders<br />-- Alzheimers Disease: Other |
| Session: |
276. Cytoskeleton Poster |
| Presentation Time: | Monday, November 12, 2001 11:00 AM-12:00 PM |
| Location: | Exhibit Hall I-4 |
| Keywords: | Gene expression, Immunohistochemistry, Amyloid, cortex |
Alzheimer's disease (AD) is a common late life dementia characterized by loss of memory and multiple cognitive impairments. Our recent investigation of gene expression profiles of transcripts in late onset AD patient brain revealed that disruption of cytoskeletal elements is one of the major cellular mechanisms involved in AD pathogenesis (Reddy et al 2000, SFN abstract #83.4). Preliminary characterization of differentially expressed cytoskeletal genes in AD brains suggested that recently described synaptopodin gene, based on its expression specificity is a potential candidate playing a role in AD pathophysiology. Northern blot analysis of 16 different normal human tissues including brain and non-CNS tissues for mRNA revealed that synaptopodin is expressed abundantly in brain, heart and skeletal muscle. Synaptopodin has two transcripts. One 4.4 kb transcript is predominantly expressed in brain, heart and skeletal muscle, while the other 5 kb transcript expressed in non-CNS tissues. Immunohistochemical examination of sections from normal human cortex using anti-synaptopodin antibodies revealed that synaptopodin has a high level of expression in cortical layers I & II, and deep layers V & VI. Synaptic loss of cortical layers I & II and V & VI are known to be implicated in AD pathogenesis. Further, Northern and Western blot analyses revealed that synaptopodin expression levels are very low both for mRNA and protein particularly in AD brains. Based on these studies, we propose that synaptopodin plays a key role in AD pathogenesis.
Supported by Alzheimer's Disease association of Oregon
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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