Table of Contents
Journal of Neurodegenerative Diseases
Volume 2016, Article ID 6163186, 6 pages
Research Article

Granulovacuolar Degeneration in Hippocampus of Neurodegenerative Diseases: Quantitative Study

1Department of Pathology, London Health Science Centre, Western University, London, ON, Canada N6A 5C1
2Department of Pathology, King Abdul-Aziz University, Jeddah, Saudi Arabia
3Department of Pathology, Schulich School of Medicine & Dentistry, Western University, London, ON, Canada N6A 5C1

Received 11 July 2016; Revised 15 September 2016; Accepted 29 September 2016

Academic Editor: Seishi Terada

Copyright © 2016 Maher Kurdi 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.


Background. Granulovacuolar degeneration (GVD) is one of the pathological features long associated with Alzheimer’s disease (AD) and normal aging. Aim. We investigate the frequency of GVDs in AD, other neurodegenerative diseases, and normal aging, with attempt to determine whether the GVD has preponderance in any particular neurodegenerative disease other than AD. Materials and Methods. A retrospective review of 111 autopsied cases with a variety of neurodegenerative diseases and 70 control cases without pathological evidence of neurodegeneration was evaluated quantitatively. The microscopic examination was applied on coronal sections of hippocampi using Hematoxylin and Eosin (H&E) and Bielschowsky silver impregnation. The mean percentage of neurons with GVDs was calculated through all sectors of Ammon’s horn for each case. Result. We found that neurons with GVD, in cases with or without neurodegenerative diseases, were found predominantly in CA1 and CA2 sectors of hippocampus. The GVD count in AD was significantly increased in CA1 and CA2 compared to other neurodegenerative cases as well as normal aging controls. In AD/LBD there was a significant increase in GVD in CA1 whereas in LBD there was no significant change in GVD. Conclusions. The frequency of GVD in AD is due to the disease process and attributes the increase for AD/LBD to the AD component.