The paper claims that chronic ozone exposure induces Alzheimer’s-like pathology, citing Aβ1-42 accumulation and tau phosphorylation. However, there’s a critical gap: no data are provided on the activation of key upstream enzymes like GSK3β (for tau) or BACE1 (for Aβ). Without this, it’s unclear whether these pathological markers result from specific AD-related pathways or are just general responses to oxidative stress. Also, Aβ detection appears limited to immunostaining, was this validated by ELISA or Western blot to confirm specificity and aggregation state? Without these validations, the claim of AD-like pathology seems premature.
