David J Loane

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Eicosapentaenoic acid confers neuroprotection in the amyloid-beta challenged aged hippocampus.

Aileen M Lynch; David J Loane; Aedín M Minogue; Rachael M Clarke; Dana Kilroy; Rachel E Nally; Oran J Roche; Florence O'Connell; Marina A Lynch (Profiled Author: David J Loane)

Trinity College Institute of Neuroscience, Physiology Department, Trinity College, Dublin 2, Ireland.
Neurobiology of aging 2007;28(6):845-55.

Among the changes that occur in the hippocampus with age, is a deficit in long-term potentiation (LTP). This impairment is associated with inflammatory changes, which are typified by increased concentration of the pro-inflammatory cytokine interleukin-1beta (IL-1beta). Activated microglia are the most likely cell source of IL-1beta, but data demonstrating an age-related increase in microglial activation is equivocal. Here we demonstrate that the age-related deficit in LTP is accompanied by increased expression of cell surface markers of activated microglia (major histocompatibility complex II and CD40) and increased IL-1beta production, and that these changes may be stimulated by interferon-gamma. Treatment of aged rats with eicosapentaenoic acid (EPA) attenuates these changes and we suggest that IL-4 mediates the action of EPA. We demonstrate that aged rats exhibit an exaggerated response to intracerebroventricular injection of beta-amyloid peptide 1-40 (Abeta). Thus Abeta inhibited LTP in aged, but not young, rats and induced a further increase in hippocampal IL-1beta concentration. Of particular significance is the demonstration that EPA protects the aged brain so that the increased vulnerability to Abeta is ameliorated in EPA-treated rats.

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