If you wrap up different kinds of furniture in enough wrapping paper, you can make them all look the same shape (12). The term “neuroinflammation” has become such a wrapping paper for an increasing number of etiologically distinct central nervous system (CNS) pathologies. As the first article (4) of this symposium explains:“Historically, the term ‘neuroinflammation’was clearly defined and denoted immune-driven pathology in the brain. Unfortunately, this clarity has diminished in recent years.” It has in fact diminished to the point that the designation “neuroinflammation” is effectively useless in practice because it denotes both true and pseudo-inflammation (5). Some recent, attentiongrabbing examples of the latter include air pollution, obesity and sleep loss (2, 3, 16).

As of August 2014, there were 6249 publications and 118 894 citations on the topic of “neuroinflammation”(Figure 1), and the increase is steep. Are most or all of these papers missing the point? Certainly not all, but the problem with a “diagnosis” that has opposite meanings in the literature cannot be solved easily in the face of thousands of publications, many of which are conflicting but cannot realistically be corrected. Therefore, although the term “neuroinflammation” seems doomed for logical reasons alone, a serious effort needs to be made to achieve clarity regarding what the findings reported in these publications mean in the light of state-of-the-art concepts (14, 15). The occurrence of classical inflammation in the CNS is the backdrop against which any consideration of “neuroinflammation” of the non-autoimmune type (9) has to be viewed and judged. Classical inflammation occurs in the CNS like in any other organ