Microglia are the resident sensors of pathology in the central nervous system. Their main function is to control tissue damage and to engage in tissue repair processes. The exact role of microglial cells in neurodegenerative disorders is unknown. Based on their expression of some molecules found in established infl ammatory disease states it has been suggested that microglia exert tissue destructive functions in Parkinson’s disease (PD). We have indeed observed a correlation between α-synuclein (αSN) deposition and MHC class II-expressing microglia in the substantia nigra in PD but it remains unclear whether there is a pathogenetic link. In addition, in the absence of infi ltrating Tcells which characterise chronic infl ammatory or autoimmune conditions, e.g. CNS infections and multiple sclerosis, classical infl ammation does not occur in PD. We therefore believe that “(micro)glial infl ammation” represents a distinct process. This idea is supported by the up-regulation of CD163 by nigral microglia in PD suggesting a possible role of resident microglia in the down-regulation of infl ammatory activity. Astrocytes in PD nigra strongly up-regulate their expression of the Hsp40 chaperone, DnaJB6 and they also increase their production of metallothioneins. They are thus in an activated state. The homocysteine-induced endoplasmic reticulum protein (Herp) may serve as a molecular link between neurodegeneration and the infl ammation-like changes observed in PD.
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