TLR4 and Alzheimer disease: The mechanism of action entails the binding of HMGB1 released from necrotic or hyper excitatory neurons with TLR4 and results in the activation of MAP kinases affecting myristoylated alanine‐rich C‐kinase substrate (MARCKS) phosphorylation resulting in the deterioration of neurites which is a fundamental landmark of AD pathology.10