Nucl Med Commun 2003 Feb;24(2):209-221
Versijpt J, Van Laere K, Dierckx RA, Dumont F, De Deyn PP, Slegers G, Korf J.
Department of Biological Psychiatry, Groningen University Hospital, the Netherlands; Division of Nuclear Medicine, Ghent University Hospital, Belgium; Department of Radiopharmacy, Ghent University, Belgium and Department of Neurology, General Hospital Middelheim, University of Antwerp and Born-Bunge Foundation, Antwerp, Belgium.
In the past few decades, our understanding of the central nervous system has evolved from one of an immune-privileged site, to one where inflammation is pathognomonic for some of the most prevalent and tragic neurodegenerative diseases.
Current research indicates that diseases as diverse as multiple sclerosis, stroke and Alzheimer's disease exhibit inflammatory processes that contribute to cellular dysfunction or loss.
Inflammation, whether in the brain or periphery, is almost always a secondary response to a primary pathogen.
In head trauma, for example, the blow to the head is the primary event.
What typically concerns the neurologist and neurosurgeon more, however, is the secondary inflammatory response that will ensue and likely cause more neuron loss than the initial injury.
This paper reviews the basic neuroinflammatory mechanisms, the potential neurotoxic mediators during activation of microglia, the brain resident macrophages, and their role in neurodegeneration.
Alzheimer's disease is taken as a prototype for exploring these mechanisms, as it expresses more than 40 inflammatory mediators, it is the most extensively studied disorder in terms of immune-related pathogenesis, and because of its importance as the most prevalent type of dementia.
Tools for the visualization of these neuroinflammatory processes, both structural and mainly functional, are critically reviewed and discussed.