Abstract

Inflammation of the central nervous system is a topic which has attracted researchers for more than 150 years. The pathologist Virchow recognized that the brain tissue is not only composed of neurons but contains a second population of cells which he termed glia. His first picture of glial cells, published in 1858 (Virchow 1958), shows cells with morphological features of activated ameboid microglia rather than astrocytes or oligodendrocytes. Since his main focus was the study of pathologic tissue, he may have recognized those glial cells which had responded to inflammation. Subsequently, pathologists described that glial cells surround damaged or dying neurons. In his extensive treatise on “the knowledge of pathologic neuroglia and their relation to degeneration of the CNS” Alois Alzheimer compared glial cells under normal conditions with those of diseased brain. He studied cases of meningitis, dementia, and epilepsy and clearly recognized that damaged and dying neurons were surrounded by ameboid glial cells. He also described that glial cells take over the space which is left after the ganglion neurons had disappeared (Alzheimer 1910). In his drawings it is evident that he had described activated ameboid microglia and reactive astrocytes. Just now we are beginning to understand that these cell types are the two major players for inflammation intrinsic to the CNS and that they exhibit a large repertoire of cellular interactions with the invading immune cells.

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