We read with great interest the recent work published in the Archives by Dorothée and colleagues1 assessing plasma levels of naturally occurring anti–amyloid-β (Aβ) IgG in Alzheimer disease (AD) and patients with posterior cortical atrophy with evidence of AD (PCA-AD). The authors elegantly pointed out a difference in the pattern of acid-dissociated total anti-Aβ IgG plasma levels, especially types 1 and 3, in PCA-AD with respect to subjects with typical AD. Interestingly, these antibodies have been proposed to play a protective role2; therefore, differences in their expression profile might imply relevant pathologic and phenotypic variability in AD. We recently reported that free plasma levels of anti-Aβ IgG in patients with AD are reduced and that therapy with acetylcholinesterase inhibitors (AChEIs) selectively increases them up to the levels expressed by healthy control subjects,3 possibly owing to an effect of phenotypic modification on T lymphocytes.4 As already emphasized,1 methodologic differences might explain the disagreement among different series. However, increased anti-Aβ IgG plasma levels in patients with AD with respect to PCA-AD might be also related to differences in AChEI treatment. In fact, the percentage of patients with PCA-AD treated with these drugs might be lower with respect to subjects with typical AD, given that AChEIs are regarded as symptomatic drugs, mainly, albeit not only, working on damaged cholinergic pathways involved in episodic memory, typically relatively preserved in patients with PCA-AD in the initial phases of the disease.5 If true, then the difference in anti-Aβ IgG levels reported by Dorothée and colleagues might simply reflect the different frequency of AChEI treatment between their 2 pathologic groups.