Abstract
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.
Highlights
Granulovacuolar degeneration (GVD) was first reported by Simchowicz in the hippocampus in cases of senile dementia in 1911 [1] and its ultrastructural characteristics were subsequently described by Hirano et al in 1968 [2]
GVD can be detected with routine histological stains such as Hematoxylin and Eosin, silver impregnation techniques, and other immunohistochemical stains including tau [16], TDP-43 [17], ubiquitin [18], GSK [16], CHMP2B [19], and Casein-kinase 1 (CK-1) [20]
GVD can be identified in nondemented patients linked to aging process or non-Alzheimer’s neurodegenerative diseases
Summary
GVD was first reported by Simchowicz in the hippocampus in cases of senile dementia in 1911 [1] and its ultrastructural characteristics were subsequently described by Hirano et al in 1968 [2]. It is depicted by intraneuronal accumulation of large membrane-bound vacuoles harboring argyrophilic granules [3]. 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. The frequency of GVD in AD is due to the disease process and attributes the increase for AD/LBD to the AD component
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