ABSTRACT
The major pathology in AD has been linked to the misfolded protein Aβ in neuritic plaques in the AD brain-related to defective clearance by macrophages in humans (Fiala et al. 2005) and microglia in transgenic models (Paresce et al. 1997). The reduced clearance of Aβ and increased inammation lead to progression of the disease(Fiala et al. 2007a; Fiala 2010).
