Maiti et al. (18) suggested that curcumin or solid lipid curcumin particles treatment could increase the levels of LC3A/B-II and Beclin-1, indicating that maintenance or restoration of heat shock proteins and regulation of autophagy–lysosomal pathways by curcumin may provide a promising strategy to degrade Aβ-aggregates from neurons in the AD brain. Here, MAP1LC3A is linked to Alzheimer disease.