AIMS: The pathology of Alzheimer's disease (AD) is characterized by the presence of amyloid plaques (APs), neurofibrillary tangles (NFTs), degenerating neurones, and an abundance of reactive astrocytes and microglia. We aim to examine the association between glia maturation factor (GMF) expression, activated astrocytes/microglia, APs and NFTs in AD-affected brain regions. METHODS: Brain sections were stained with Thioflavin-S to study AD pathology and sequentially immunolabeled with antibodies against GMF, glial fibrillary acidic protein (marker for reactive astrocytes), and Ionized calcium binding adaptor molecule 1 (Iba-1, marker for activated microglia) followed by visualization with avidin-biotin peroxidase complex. RESULTS: Our double immunofluorescence labelling with cell-specific markers demonstrated the glial localization of GMF. The immunohistochemical data showed that APs and NFTs are associated with increased expression of GMF in reactive glia of AD brains compared with non-AD controls. CONCLUSIONS: This is the first report that shows GMF, a mediator of central nervous system inflammation, is expressed in the brain regions affected in AD and that GMF is mainly localized in reactive astrocytes surrounding APs/NFTs. The distribution of GMF-immunoreactive cells in and around Thioflavin-S stained APs and NFTs suggests involvement of GMF in inflammatory responses through reactive glia and a role of GMF in AD pathology.
AIMS: The pathology of Alzheimer's disease (AD) is characterized by the presence of amyloid plaques (APs), neurofibrillary tangles (NFTs), degenerating neurones, and an abundance of reactive astrocytes and microglia. We aim to examine the association between glia maturation factor (GMF) expression, activated astrocytes/microglia, APs and NFTs in AD-affected brain regions. METHODS: Brain sections were stained with Thioflavin-S to study AD pathology and sequentially immunolabeled with antibodies against GMF, glial fibrillary acidic protein (marker for reactive astrocytes), and Ionized calcium binding adaptor molecule 1 (Iba-1, marker for activated microglia) followed by visualization with avidin-biotin peroxidase complex. RESULTS: Our double immunofluorescence labelling with cell-specific markers demonstrated the glial localization of GMF. The immunohistochemical data showed that APs and NFTs are associated with increased expression of GMF in reactive glia of AD brains compared with non-AD controls. CONCLUSIONS: This is the first report that shows GMF, a mediator of central nervous system inflammation, is expressed in the brain regions affected in AD and that GMF is mainly localized in reactive astrocytes surrounding APs/NFTs. The distribution of GMF-immunoreactive cells in and around Thioflavin-S stained APs and NFTs suggests involvement of GMF in inflammatory responses through reactive glia and a role of GMF in AD pathology.
Authors: R M Baldwin; M Garratt-Lalonde; D A E Parolin; P M Krzyzanowski; M A Andrade; I A J Lorimer Journal: Oncogene Date: 2006-05-11 Impact factor: 9.867
Authors: Peter T Nelson; Erin L Abner; Frederick A Schmitt; Richard J Kryscio; Gregory A Jicha; Karen Santacruz; Charles D Smith; Ela Patel; William R Markesbery Journal: J Neuropathol Exp Neurol Date: 2009-07 Impact factor: 3.685