Neuroinflammation was once the purvey of those of us studying infectious processes in the central nervous system (CNS) or other forms of inflammation resulting from the adaptive immune response such as the animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). Neurodegenerative diseases were considered to be just that, degenerative, with any inflammation the byproduct of degeneration and its role to 'clean up' the destruction. The first edition of Neuroinflammation: Mechanisms and Management was published in 1998 and brought together work supporting the concept that in many of the degenerative diseases, activation of the CNS cells of the innate immune system, the microglia, and the subsequent inflammatory response preceded (causes) neuronal degeneration and/or contributed to ongoing destruction. This second edition, 5 years later, continues this theme.
The book is divided into two parts, I. inflammatory mechanisms and II. specific pathologic conditions and diseases. Microglia, as that enigmatic cell of the CNS, with its flexible morphology, antigenicity and functionality as well as its mobility and proliferative capacity opens the book in the first chapter. Interestingly, the role(s) of microglia in the normal CNS is still the topic for much debate but a consensus is slowly building that it is the key 'target' for pharmacological approaches for halting or preventing progressive neurodegenerative diseases. The microglia is 'the' cell of importance in virtually all chapters. Other chapters dealing with mechanisms address apoptosis versus necrosis as types of cell death, chemokines, kinases and nitric oxide as mediators, all produced by microglia (as well as other cells).
Stroke and traumatic brain injury (TBI) (spinal cord injury) are discussed in a chapter each. There are six chapters on Alzheimer's disease, three on multiple sclerosis, and one each on Parkinson's and Huntington's diseases. One strength of the book is that there are chapters on existing and new experimental models of most of the diseases discussed. This allows the reader to compare studies and draw his/her own conclusions about the relevance of the models to the human disease. There is also a very interesting chapter on in vivo imaging (using radiolabelled ligands for the peripheral benzodiazepine receptors) in neuroinflammation and degeneration. Unfortunately this chapter could have used some careful editing as there were several minor and one major error in sentence structure.
The book is well balanced not only with respect to models versus human disease but also with respect to opinions. I suggested above that a consensus was building that targeting the microglia would be good for neurodegenerative diseases, implying of course a causal role for it in disease. Not all contributors agree with this concept. Wenk and Hauss-Wegrzyniak make it quite clear at the beginning of their chapter that they do not believe 'neuroinflammation causes Alzheimer's disease'. They present an animal model which 'provides evidence that inflammation develops in response to existing genetically determined conditions within brains of AD patients'. How compelling this evidence is rests with the reader.
Finally, there are several chapters dealing with possible therapeutic approaches to neurodegenerative diseases. This book is highly recommended not just for those scientists working in the area of neurodegenerative diseases but perhaps most importantly for those, like myself, who have in the past tended to think of neuroinflammation as being driven principally by the peripheral adaptive immune system.
