HMGB1 and Alzheimer disease: Thus, given the reversibility of the AIE-induced acceleration of basal forebrain cholinergic neuron loss in the present study, coupled with little evidence of cell death in clinical AD studies and preclinical AD models (Wu et al., 2005; Stepanichev et al., 2017), it is plausible that targeting neuroinflammation through blockade of proinflammatory HMGB1 signaling, particularly during the early stages of AD progression, may represent a novel therapeutic approach for the treatment of AD.