We next examined the implication of proinflammatory response on the accumulation of hyperphosphorylated tau (pTau) (Figure 6b,d), one of the major hallmarks involved in the progression of tauopathies and CNS disorders including AD, PD, and dementia.[5] Our data showed that there was a slight increase in the models of PM2.5‐treated neurons and astrocytes (Co‐PBM) (2.3‐fold) compared to the nontreated group (Co‐Con). The gene discussed is MAPT; the disease is Alzheimer disease.