Glia Maturation Factor Expression in Entorhinal Cortex of Alzheimer’s Disease Brain

被引:0
|
作者
Ramasamy Thangavel
Duraisamy Kempuraj
Deirdre Stolmeier
Poojya Anantharam
Mohammad Khan
Asgar Zaheer
机构
[1] Veterans Affairs Health Care System,Division of Neurochemistry and Neurobiology, Department of Neurology, Carver College of Medicine
[2] The University of Iowa Hospitals and Clinics,undefined
来源
Neurochemical Research | 2013年 / 38卷
关键词
Alzheimer’s disease; Amyloid plaques; Entorhinal cortex; Glia maturation factor; Neurofibrillary tangles; Neuroinflammation;
D O I
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学科分类号
摘要
Alzheimer’s disease (AD) is characterized by the presence of neuropathological lesions containing amyloid plaques (APs) and hyperphosphorylated Tau containing neurofibrillary tangles (NFTs) and is associated with neuroinflammation and neurodegeneration. Entorhinal cortex (Brodmann’s area 28) is involved in memory associated functions and is one of the first brain areas targeted to form the neuropathological lesions and also severely affected cortical region in AD. Glia maturation factor (GMF), a central nervous system protein and a proinflammatory molecule is known to be up-regulated in the specific areas of AD brain. Our previous immunohistochemical studies using temporal cortex showed that GMF is expressed in the vicinity of APs and NFTs in AD brains. In the present study, we have analyzed the expression of GMF and its association with APs and NFTs in the entorhinal cortex of AD brains by using immunohistochemistry combined with thioflavin-S fluorescence labeling methods. Results showed that GMF immunoreactive glial cells, glial fibrillary acidic protein labeled reactive astrocytes and ionized calcium binding adaptor molecule-1 labeled activated microglia were increased in the entorhinal cortical layers especially at the sites of 6E10 labeled APs and Tau containing NFTs. In conclusion, increased expression of GMF by the glial cells in the entorhinal cortex region, and the co-localization of GMF with APs and NFTs suggest that GMF may play important proinflammatory roles in the pathogenesis of AD.
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页码:1777 / 1784
页数:7
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