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P2–006: A glucocorticoid–amyloid precursor protein connection
Author(s) -
Catania Caterina,
Sotiropoulos Ioannis,
Silva Rui,
Sousa Nuno,
Almeida Osborne F.X.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.843
Subject(s) - glucocorticoid , amyloid precursor protein , hippocampal formation , neuroprotection , endocrinology , medicine , hippocampus , neurotoxicity , dexamethasone , synaptic plasticity , neuroscience , biology , chemistry , alzheimer's disease , toxicity , receptor , disease
ferences in the cellular inflammatory response (reactive astrocytes & microglia), in beta amyloid 1-42 deposition, and in the presence of C. pneumoniae in the brain. Results: Initial results indicate that, with antibiotic treatment, astrocytic activation was more prominent at 3 months post-infection as compared to 6 months post-infection. Animals infected and treated at 7-21 days post-infection, demonstrated numerous reactive astrocytes at 3 months as compared to 6 months, which showed reduced numbers of reactive astrocytes. Intriguingly, in animals treated at 7-21 days post-infection, immunolabeling for C. pneumoniae in the brains was comparable between 3 months and 6 months, although the number of amyloid plaques on average was greater in the 3 month animals. With treatment delayed until 56-70 days post-infection, less cellular reactivity was recognized in both the 3 and 6 month animals, although labeling for C. pneumoniae and amyloid was still prominent, especially in the 6 month animals. Conclusion: These data suggest that early antibiotic treatment, 7-21 days post-infection, may help to modulate the cellular inflammatory processes following C. pneumoniae infection, which ultimately may affect the extent of infection and subsequent amyloid deposition in the mouse brain.