Inflamed in the brain

Neuroinflammatory Mechanisms in Alzheimer's Disease: Basic and Clinical Researchedited by Joseph RogersBirkhauser Verlagm, 2001. $149 (261 pages)ISBN 3-7643-6074-7Fifteen years ago, the concept that inflammation might participate in central nervous system diseases was largely limited to demyelinating disorders and some infectious causes. Championed by a few individuals in the late 1980s and early 1990s, there is now widespread acceptance that inflammation-related changes are prominent in the Alzheimer's brain and might play a role in disease pathogenesis. According to Neuroinflammatory Mechanisms in Alzheimer's Disease, the neuroinflammation of Alzheimer's disease (AD) is ‘a locally-induced, aspecific, chronic inflammatory response without influx of leukocytes’ (p. 68). Primary features of this response include activated glial cells associated with neuritic plaques and local production of inflammatory mediators. More recently, similar features have been recognized in other neurodegenerative diseases, including Parkinson's disease and amyotrophic lateral sclerosis. Joseph Rogers, one of the original crusaders for neuroinflammation in AD, provides us with a rich compendium that emphasizes many facets of the process.Written by founding and long-term proponents of neuroinflammation in AD, overviews of basic and clinical findings at the start of the volume go far beyond typical introductions. For example, an 11-page table summarizing nearly all the literature related to inflammatory markers in AD provides an essential reference guide for researchers. In the clinical research overview, Patrick McGeer and colleagues present a comprehensive and lucid critique of epidemiological studies that suggest benefits of anti-inflammatory therapy in AD. Similar to the preceding chapter, this section is required reading for anyone curious about the evidence for such therapies.The remaining 11 chapters of the volume, categorized as ‘Topics of Special Interest’, are written by experts in their respective fields. There is significant uniformity among the chapters with regard to depth and reliance on recent literature, giving a balanced impression for the reader. Although a wide range of subjects is covered, each is presented in a well-rounded manner with no attempt to emphasize one mechanism over others. This is quite appropriate given the complexity inherent to neuroinflammation and AD. Areas of particular emphasis include chapters on complement components, interactions of β-amyloid with molecular and glial elements, perspectives on relationships between inflammatory mediators and oxidant stress, and cellular constituents of neuroinflammation including microglia and neurons. In the final chapter, Caleb Finch and colleagues emphasize that ‘neuroinflammatory processes observed in AD should be considered in the context of similar, but less intense changes in brain during normal aging’ (p. 249) as well as age-related changes in peripheral organs and systems.As in most edited collections, some subjects commonly associated with AD are not well covered. Missing from this volume are chapters devoted to proinflammatory cytokines other than interleukin-6, the role of astrocytes and potential interactions between neuroinflammation and vascular changes found in AD. In addition, the field of neuroinflammation is moving at a rapid pace. Thus, very current and exciting findings related to Aβ vaccination, the association between AD and genetic polymorphisms in cytokine genes, application of transgenic mouse models, and alternate mechanisms for anti-inflammatory drug actions are only briefly mentioned. Nevertheless, the even-handedness, depth and clarity of writing in this volume warrant a strong recommendation for students of neuroinflammation in AD and other neurodegenerative diseases.