Table of Contents
Journal of Neurodegenerative Diseases
Volume 2014 (2014), Article ID 938530, 14 pages
http://dx.doi.org/10.1155/2014/938530
Research Article

Differential Changes in Postsynaptic Density Proteins in Postmortem Huntington’s Disease and Parkinson’s Disease Human Brains

1Department of Physiology, Centre for Brain Research, University of Auckland, Private Bag 92019, Auckland, New Zealand
2Department of Anatomy with Radiology, Centre for Brain Research, University of Auckland, Private Bag 92019, Auckland, New Zealand
3School of Pharmacy, Centre for Brain Research, University of Auckland, Private Bag 92019, Auckland, New Zealand

Received 13 August 2013; Revised 14 October 2013; Accepted 29 October 2013; Published 16 January 2014

Academic Editor: Eng King Tan

Copyright © 2014 C. Fourie et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

NMDA and AMPA-type glutamate receptors and their bound membrane-associated guanylate kinases (MAGUKs) are critical for synapse development and plasticity. We hypothesised that these proteins may play a role in the changes in synapse function that occur in Huntington’s disease (HD) and Parkinson’s disease (PD). We performed immunohistochemical analysis of human postmortem brain tissue to examine changes in the expression of SAP97, PSD-95, GluA2 and GluN1 in human control, and HD- and PD-affected hippocampus and striatum. Significant increases in SAP97 and PSD-95 were observed in the HD and PD hippocampus, and PSD95 was downregulated in HD striatum. We observed a significant increase in GluN1 in the HD hippocampus and a decrease in GluA2 in HD and PD striatum. Parallel immunohistochemistry experiments in the YAC128 mouse model of HD showed no change in the expression levels of these synaptic proteins. Our human data show that major but different changes occur in glutamatergic proteins in HD versus PD human brains. Moreover, the changes in human HD brains differ from those occurring in the YAC128 HD mouse model, suggesting that unique changes occur at a subcellular level in the HD human hippocampus.