Synaptic Degeneration in Alzheimer's Disease

Chang, R., Etheridge, N., Nouwens, A. and Dodd, P. (2011). Synaptic Degeneration in Alzheimer's Disease. In: Australian Neuroscience Society Annual Meeting, Auckland, New Zealand, (). 31 January - 3 February 2011.

Author Chang, R.
Etheridge, N.
Nouwens, A.
Dodd, P.
Title of paper Synaptic Degeneration in Alzheimer's Disease
Conference name Australian Neuroscience Society Annual Meeting
Conference location Auckland, New Zealand
Conference dates 31 January - 3 February 2011
Publication Year 2011
Sub-type Poster
Language eng
Abstract/Summary Purpose: Synaptic dysfunction occurs early in Alzheimer’s disease (AD) and is recognized as a primary pathologic target for AD treatment. Synapse degeneration or dysfunction contributes to clinical signs of dementia through altered neuronal communication and the degree of synaptic loss strongly correlates with cognitive impairment. The exact molecular mechanisms underlying synaptic degeneration are still relatively unclear; therefore, identifying abnormally expressed synaptic proteins in AD brain will help to elucidate those mechanisms and can lead to the identification of therapeutic targets that might slow AD progression. Methods: In the present study, synaptosomal fractions from post-mortem human brain tissue of AD (n = 6) and control (n = 6) were compared using 2D-differential in gel electrophoresis. AD pathology is region specific; human subjects can be highly variable in age, medication and other factors. Consequently, within each diseased state, hippocampus was compared with two relatively spared areas (motor and occipital cortices). Proteins exhibiting significant changes in their expression were identified (≥20% change, Newman-Keuls P-value <0.05) using either MALDI-TOF or ESI-QTOF mass spectrometry. Results: Using this proteomics approach, 70 synaptic proteins were found to be differentially regulated in hippocampus of AD brain when compared to controls. These proteins are involved regulating different cellular functions including energy metabolism, signal transduction, vesicle transport, structural and antioxidant function. Conclusion: This study showed that synaptic proteins in human AD brain are significantly different from those in control brain. Of the proteins identified in this study, a number have been studied in animal models, but only a few in human brain tissues. The functions regulated by these synaptic proteins with respect to AD will be discussed.
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status UQ

 
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Created: Thu, 13 Oct 2011, 09:44:25 EST by Dr Amanda Nouwens on behalf of Aust Institute for Bioengineering & Nanotechnology