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Inflammation in Alzheimer's disease: relevance to pathogenesis and therapy

Elina Zotova1 email, James AR Nicoll1,2 email, Raj Kalaria3 email, Clive Holmes1,4 email and Delphine Boche1 email

Division of Clinical Neurosciences, School of Medicine, University of Southampton, Mailpoint 806, Level D, South Pathology Block, Southampton General Hospital, Southampton, SO16 6YD, UK

Neuropathology, Department of Cellular Pathology, Southampton University Hospitals NHS Trust, Southampton, SO16 6YD, UK

Institute for Ageing and Health, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne NE4 5PL, UK

Memory Assessment Centre, Moorgreen Hospital, Hampshire Partnership Trust, Southampton, SO30 3JB, UK

author email corresponding author email

Alzheimers Res Ther 2010, 2:1doi:10.1186/alzrt24

Published: 22  January  2010

Abstract

Evidence for the involvement of inflammatory processes in the pathogenesis of Alzheimer's disease (AD) has been documented for a long time. However, the inflammation hypothesis in relation to AD pathology has emerged relatively recently. Even in this hypothesis, the inflammatory reaction is still considered to be a downstream effect of the accumulated proteins (amyloid beta (Aβ) and tau). This review aims to highlight the importance of the immune processes involved in AD pathogenesis based on the outcomes of the two major inflammation-relevant treatment strategies against AD developed and tested to date in animal studies and human clinical trials - the use of anti-inflammatory drugs and immunisation against Aβ.

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