Boon BDC, et al. - Given that recent studies suggest a prominent role for neuroinflammation in the spreading of tau pathology, researchers investigated if an atypical spreading of pathology in Alzheimer’s disease (AD) is related to an atypical distribution of neuroinflammation. In the selected typical and atypical AD cases, quantification of the presence of amyloid-beta (N-terminal; IC16), pTau (AT8), reactive astrocytes (GFAP), microglia (Iba1, CD68, and HLA-DP/DQ/DR), and complement factors (C1q, C3d, C4b, and C5b-9) was done using image analysis. Findings revealed a different localization of neuroinflammatory markers and amyloid-beta plaques between AD phenotypes. They identified neuroinflammation might be a crucial link between amyloid-beta deposits, tau pathology, and clinical symptoms as these markers indicated the atypical distribution of tau pathology in atypical AD.