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Plasma Anti–Amyloid-β Autoantibodies in All Alzheimer Disease Types—Reply

Guillaume Dorothée, PhD; Leonardo Cruz de Souza, MD, PhD; Marie Sarazin, MD, PhD; Pierre Aucouturier, PhD
Arch Neurol. 2012;69(11):1525-1527. doi:10.1001/archneurol.2012.2779.
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The question raised by Tremolizzo and colleagues relates to their recent observation that treatments with acetylcholinesterase inhibitors could impact the circulating levels of anti–amyloid β (Aβ) antibodies.1 As a matter of fact, our observation of significant differences in anti-Aβ antibody levels between patients with typical Alzheimer disease (AD) and patients with posterior cortical atrophy with evidence of AD (PCA-AD)2 could have been influenced by external factors including treatments. However, this possibility may be ruled out for the following 2 main reasons.

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Figure. Serum free anti–amyloid-β antibody levels in patients with typical Alzheimer disease (AD) and those with atypical AD (posterior cortical atrophy with evidence of AD [PCA-AD]) and control subjects. NS indicates not significant; OD, optical density.




November 1, 2012
Lucio Tremolizzo, MD, PhD; Elisa Conti, PhD; Ildebrando Appollonio, MD; Carlo Ferrarese, MD, PhD
Arch Neurol. 2012;69(11):1525-1527. doi:10.1001/2013.jamaneurol.6.
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