Traditionally the brain has been viewed as being an immune-privileged organ. However, endogenous stimuli such as the presence of misfolded or aggregated proteins, as well as systemic inflammatory events may lead to the activation of microglial cells, the brain´s innate immune system, and, subsequently, to neuroinflammation. Alzheimer's disease, the leading cause of dementia, is characterized by amyloid beta deposition and tau hyperphosphorylation. Neuroinflammation in Alzheimer's disease has been identified as major contributor to disease pathogenesis. Once activated, microglia release several pro and anti-inflammatory mediators of which several affect the function and structure of the brain. Modulation of this microglial activation in Alzheimer's disease might open new therapeutic avenues.