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Increased expression of the Nogo receptor in the hippocampus and its relation to the neuropathology in Alzheimer's disease

Summary Alzheimer's disease (AD) is the most prevalent cause of dementia in human beings. Its best-known pathologic feature is the presence of senile plaques and neurofibrillary tangles in the brain. Nogo-66 receptor (NgR) is believed to contribute to the inhibitory activities of axon regenerat...

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Published in:Human pathology 2007-03, Vol.38 (3), p.426-434
Main Authors: Zhu, Hong-Yan, MS, Guo, Hou-Fu, BS, Hou, Hai-Long, MS, Liu, Ya-Jing, MS, Sheng, Shu-Li, MD, Zhou, Jiang-Ning, MD, PhD
Format: Article
Language:English
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Summary:Summary Alzheimer's disease (AD) is the most prevalent cause of dementia in human beings. Its best-known pathologic feature is the presence of senile plaques and neurofibrillary tangles in the brain. Nogo-66 receptor (NgR) is believed to contribute to the inhibitory activities of axon regeneration after injury. This study investigated the expression of NgR in the hippocampus and its relation to the pathologic changes of AD using immunohistochemistry and double-labeling immunofluorescence methods. The results showed that NgR immunoreactivity was present in more than 50% of the pyramidal layer cells of the CA1 to CA4 subfields of the hippocampus. No significant difference was observed in the number of NgR immunopositive cells in the CA1 to CA4 subfields between patients with AD and control subjects, whereas the ratio of NgR immunopositive cells to the total number of pyramidal layer cells was revealed to be significantly higher in the CA1 and CA2 subfields of the hippocampus of patients with AD than that in the same region of the control subjects. Moreover, high numbers of AT-8 immunopositive cells were found to be double-labeled with NgR in the CA1 subfields of patients with AD, whereas only few NgR deposits were observed in the senile plaques of the hippocampus in these patients. These results suggest that NgR may be related to the formation of tangles in AD.
ISSN:0046-8177
1532-8392
DOI:10.1016/j.humpath.2006.09.010