Korean J Anat.  2005 Oct;38(5):451-459.

Immunohistochemical Study on GTP-binding Rab6 Expression in the Hippocampal Cortices of the Alzheimer Brain

Affiliations
  • 1Department of Anatomy and Neurosciences, Eulji University School of Medicine, Korea. tkbaik@eulji.ac.kr
  • 2Department of Neurology, Maryknoll General Hospital, Korea.

Abstract

The ras-related GTP binding protein, rab6, is located in late Golgi compartment. Modulation of beta-and gamma-secretase activity may lead to production of beta-amyloid fragments that are ultimately deposited in senile plaques at the brain of Alzheimer patients. Because modulation of rab6-mediated intracellular transport has been known to affect amyloid precursor protein (APP) processing, we investigated the rab6 immunoreactivity on the hippocampal neurons in the Alzheimer brains, according to the pathological staging of the disease. A total of 30 brains were used for this study. Campbell's silver stain for beta-amyloid and immunohistochemistry for rab6 protein were employed. The cortices of the hippocampal formation and the neighboring temporal neocortex were observed. The results are obtained as follows: 1. In normal elderly brains, no amyloid plaque is seen. In Alzheimer brains, a number of amyloid plaques are seen at the temporal neocortex and dentate gyrus. 2. In normal elderly brains, the perikaria of the pyramidal cells at the CA1 sector shows weak rab6 immunoreactivity. At the CA2 and CA3 sectors, trace immunoreactivity is observed in the pyramidal cells. 3. In preclinical Alzheimer brains, the perikaria of the pyramidal cells at the CA1 sector shows moderate rab6 immunoreactivity and the cells at the CA2 sector show weak immunoreactivity. A weak to moderate imunoreactivity is seen in the pyramidal cells of the CA3 sector. 4. In clinical Alzheimer brains, the pyramidal cells at the CA1 and CA3 sectors show strong rab6 immunoreactivity, but the cells at the CA2 sector shows moderate immunoreactivity. It is suggested that alteration of intracellular protein transport caused by abnormal rab6 activity may modulate amyloid precursor protein processing, which results in beta-amyloid production.

Keyword

Rab6 protein; Amyloid precursor protein; beta-amyloid; Alzheimer brain

MeSH Terms

Aged
Amyloid
Amyloid Precursor Protein Secretases
Brain*
Dentate Gyrus
GTP-Binding Proteins
Hippocampus
Humans
Immunohistochemistry
Neocortex
Neurons
Plaque, Amyloid
Protein Transport
Pyramidal Cells
Silver
Amyloid
Amyloid Precursor Protein Secretases
GTP-Binding Proteins
Silver
Full Text Links
  • KJA
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2022 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr