Inflammation has long been proposed as having a role in AD (Alzheimer's disease), although it remains unclear whether inflammation represents a cause or consequence of AD. Evidence from the clinical setting in support of a role for inflammation in AD includes increased expression of inflammatory mediators and microglial activation in the post-mortem AD brain. Also, epidemiological studies on AD patients under long-term treatment with non-steroidal anti-inflammatory drugs suggest some benefits, although recent prospective trials showed no effect. Furthermore, in AD patients, infection and other systemic inflammatory events worsen symptoms. Finally, several inflammatory genes are associated with increased risk of AD. Therefore, to elucidate the underlying mechanisms of AD and the role of inflammation, researchers have turned to experimental models and here we present a short overview of some key findings from these studies. Activation of microglia is seen in various transgenic models of AD, with both a protective role and a detrimental role being ascribed to it. Early microglial activation is probably beneficial in AD, through phagocytosis of amyloid β-peptide. At later stages however, pro-inflammatory cytokine release from microglia could contribute to neuronal demise. A better understanding of microglial phenotype at the various stages of AD is therefore still required. Although most studies suggest a detrimental role for pro-inflammatory cytokines such as interleukin-1 and tumour necrosis factor in AD, contradictory findings do exist. Age-related and differential cellular expression of these inflammatory mediators is probably a key determinant of their exact contribution to AD. In conclusion, there is no doubt that inflammatory processes are part of the pathophysiology of AD, but a better understanding of the exact contribution at different stages of the disease process is still required before appropriate treatment strategies can be devised.
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Conference Article|
July 20 2011
Assessing the contribution of inflammation in models of Alzheimer's disease
Hannah Johnston;
Hannah Johnston
1Faculty of Life Sciences, University of Manchester, AV Hill Building, Manchester M13 9PT, U.K.
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Herve Boutin;
Herve Boutin
1Faculty of Life Sciences, University of Manchester, AV Hill Building, Manchester M13 9PT, U.K.
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Stuart M. Allan
Stuart M. Allan
1
1Faculty of Life Sciences, University of Manchester, AV Hill Building, Manchester M13 9PT, U.K.
1To whom correspondence should be addressed (email stuart.allan@manchester.ac.uk).
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Publisher: Portland Press Ltd
Received:
February 28 2011
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2011 Biochemical Society
2011
Biochem Soc Trans (2011) 39 (4): 886–890.
Article history
Received:
February 28 2011
Citation
Hannah Johnston, Herve Boutin, Stuart M. Allan; Assessing the contribution of inflammation in models of Alzheimer's disease. Biochem Soc Trans 1 August 2011; 39 (4): 886–890. doi: https://doi.org/10.1042/BST0390886
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