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Detecting both current and prior Helicobacter pylori infection is important to assess its impact on dementia
Author(s) -
RoubaudBaudron Claire,
Mégraud Francis,
Salles Nathalie,
Dartigues JeanFrançois,
Letenneur Luc
Publication year - 2019
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.12.020
Subject(s) - population , cartography , geography , medicine , environmental health
We read with great interest the article written by Fani et al. on the association between Alzheimer’s disease and Helicobacter pylori infection studied on a population-based cohort (Rotterdam study) [1]. The authors did not find any association between the two diseases, that is, H. pylori infection was not associated with an increased dementia incidence after a mean follow-up of 10 years in more than 4000 participants. As the authors mentioned in their article, we previously carried out a similar study (PAQUID—“Personnes Ag ees QUID” study) on 603 noninstitutionalized individuals aged 65 years and older living in the southwest of France followed from 1989 to 2008 with opposite conclusions [2]. Apart from the plausible causes mentioned by Fani et al. explaining this discrepancy, for example, the difference in infection prevalence, mean age of the study population, or strain virulence, an alternative explanation can be provided. Indeed, although H. pylori infection was diagnosed by ELISA technique in the Rotterdam study, in our study, we combined the same ELISA (Pyloriset EIA-G III ELISA; Orion Diagnostica, Espoo, Finland) with an immunoblot (HELICOBLOT 2.1, Genelabs Diagnostics, Singapore) able to detect long-lasting antibodies [3,4]. Immunoblot is able to detect the presence of antibodies to H. pylori proteins including cytotoxinassociated antigen A [CagA], which is a virulent factor and triggers a strong immune response. Antibodies to CagA may prevail longer after eradication (more than 10 years in some of cases) [5], in contrast to the antibodies detected by ELISAwhich may disappear 1 year or more after an eventual eradication or after development of extensive atrophy (gastric atrophy may be associated with a disappearance of H. pylori) [6,7]. In the PAQUID study, we considered patients with a positive ELISA or immunoblot as infected: 27.6% of “infected patients” were ELISA negative and immunoblot positive. Among immunoblot-positive subjects, 87% were CagA positive. When considering only the subjects with a positive ELISA as “infected” (as in Fani et al.), the risk of developing dementia over the 20-year follow-up dropped from 1.46 (95% confidence interval 1.01–2.11) to 1.27