[Skip to Content]
Sign In
Individual Sign In
Create an Account
Institutional Sign In
OpenAthens Shibboleth
[Skip to Content Landing]
Views 226
Citations 0
Nov 2012

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

Author Affiliations

Author Affiliations: Section of Neurology, Department of Neuroscience and Biomedical Technologies, University of Milano–Bicocca, S Gerardo Hospital, Monza, Italy.

Arch Neurol. 2012;69(11):1525-1527. doi:10.1001/2013.jamaneurol.6

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.

Back to top
Article Information

Correspondence: Dr Tremolizzo, Section of Neurology, Department of Neuroscience and Biomedical Technologies, University of Milano–Bicocca, S Gerardo Hospital, via Pergolesi 33–20900 Monza, Italy (lucio.tremolizzo@unimib.it).

Conflict of Interest Disclosures: None reported.

Dorothée G, Bottlaender M, Moukari E,  et al.  Distinct patterns of antiamyloid-β antibodies in typical and atypical Alzheimer disease [published online June 18, 2012].  Arch NeurolPubMedArticle
Dodel R, Balakrishnan K, Keyvani K,  et al.  Naturally occurring autoantibodies against beta-amyloid: investigating their role in transgenic animal and in vitro models of Alzheimer's disease.  J Neurosci. 2011;31(15):5847-5854PubMedArticle
Conti E, Galimberti G, Tremolizzo L,  et al.  Cholinesterase inhibitor use is associated with increased plasma levels of anti-Aβ 1-42 antibodies in Alzheimer's disease patients.  Neurosci Lett. 2010;486(3):193-196PubMedArticle
Reale M, Iarlori C, Gambi F, Feliciani C, Isabella L, Gambi D. The acetylcholinesterase inhibitor, Donepezil, regulates a Th2 bias in Alzheimer's disease patients.  Neuropharmacology. 2006;50(5):606-613PubMedArticle
Aresi A, Giovagnoli AR. The role of neuropsychology in distinguishing the posterior cortical atrophy syndrome and Alzheimer's disease.  J Alzheimers Dis. 2009;18(1):65-70PubMed