mouse model that early microglial alternative activation around amyloid plaques showed neuroprotective capabilities, however at later stages the inter-plaque activated microglial displayed a classic phenotype with pro-inflammatory cytokine release that could contribute to neuronal demise. A better understanding of microglial phenotype at the various stages of AD in human brain is still required. Methods: RT-PCR, western blots and immunostaining were performed in non-demented controls and clinically diagnosed mild (Braak II) to severe (Braak V-VI) AD cases. Results: As expected, our molecular and cellular data demonstrated the existence of a neuroinflammatory process even at early Braak stages. However, the active microglial cells in Braak II samples displayed a preferential alternative phenotype. On the contrary, Braak Vand/or VI samples displayed the classic microglial activation state, characterized by the expression of cytotoxic TNF-alpha and FAS-L. In the same Braak V/VI samples, we also observed a consistent reduction in the expression of death receptor antagonists (FLIP-L, FAIM-L and Life Guard). Also as expected from previous results, we have found a significant increase in the presence of CD3 positive cells in AD samples. Noteworthy, these CD3 positive lymphocytes were polarized to a Th1 stage. Conclusions: These data were consistent with the possible implication of the classic microglial activation on the neurodegenerative process of AD. Also, the presence of different oligomeric Abeta forms could trigger these classic microglial response.