Affiliations: [a] Fatebenefratelli Foundation for Health Research and Education, AFaR Division, “San Giovanni Calibita” Fatebenefratelli Hospital, Rome, Italy | [b] Department of Human Genetics, University of Michigan Medical School, Ann Arbor, MI, USA | [c] Department of Neuroimaging, IRCCS San Raffaele Pisana, Rome, Italy | [d] Don Carlo Gnocchi Foundation ONLUS, Italy | [e] Istituto Scienze e Tecnologie della Cognizione (ISTC) – CNR, Department of Neuroscience, Fatebenefratelli Hospital, Rome, Italy | [f] Laboratorio di Neurodegenerazione, IRCCS San Raffaele Pisana, Italy
Correspondence:
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Correspondence to: Mariacarla Ventriglia, PhD, Department of Neuroscience, Fatebenefratelli Foundation, AFaR Division, 00186 Rome, Italy. Tel.: +39 06 6837 385; Fax: +39 06 6837 300; [email protected]
Abstract: To evaluate whether zinc levels in serum, plasma, and cerebrospinal fluid are altered in Alzheimer’s disease (AD), we performed meta-analyses of 27 studies on the topic published from 1983 to 2014. The subjects’ sample obtained by merging studies was a pooled total of 777 AD subjects and 1,728 controls for serum zinc studies, 287 AD subjects and 166 controls for plasma zinc, and of 292 AD subjects and 179 controls for CSF zinc. The main result of this meta-analysis is the very high heterogeneity among the studies either in demographic terms or in methodological approaches. Although we considered these effects in our analyses, the heterogeneity persisted and it has to be taken into account in the interpretation of the results. Our meta-analysis indicated that serum zinc appears significantly decreased in AD patients compared with healthy controls, and this result is confirmed when serum and plasma studies were analyzed together. If we considered the age-matched studies, the meta-analysis carried out on only six studies showed no significant difference in zinc levels between AD and healthy controls (SMD =−0.55, 95% CI (−1.18; 0.09); p = 0.094; I2 = 91%). In the light of these findings, we speculated about the possibility that the decreases observed could indicate a possible dietary zinc deficiency and we suggested that the possible involvement of zinc alterations in AD may have an interplay with copper metabolism.
