Title:Testosterone, Estradiol, and Sex Hormone-Binding Globulin in Alzheimer’s Disease: A Meta-Analysis
VOLUME: 13 ISSUE: 3
Author(s):Jing Xu, Lei-Lei Xia, Ning Song, Sheng-Di Chen and Gang Wang
Affiliation:Department of Neurology & Institute of Neurology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China., Department of Neurology & Institute of Neurology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Keywords:Alzheimer’s disease, biomarkers, estradiol, meta-analysis, sex hormone-binding globulin, testosterone.
Abstract:Background: Previous studies suggested that plasma sex hormones may be
implicated in the pathogenesis of Alzheimer’s disease (AD). However, the relationship
between sex hormones and AD remains unclear. Objective: To systematically review
and quantitatively analyze studies observing plasma total testosterone (TT), estradiol
(E2), and sex hormone-binding globulin (SHBG) levels among AD patients. Methods: Medline, EMBASE, the Cochrane
Library, and PsycINFO® were searched for studies published prior to March 28th, 2014. Published studies that reported
plasma levels of TT, E2, and SHBG in AD and matched controls were included in the present meta-analysis. Results:
Meta-analysis was performed using the random effects model, expressing continuous outcomes as the mean difference
(MD) between AD and control populations. The 95% confidence intervals (CI) were also calculated. No differences were
found in plasma levels of TT and E2 between AD and matched controls (TT MD -0.17 nmol/l, 95%CI -0.54, 0.20; E2 MD
-1.16 pmol/l, 95%CI -9.85, 6.83). Plasma levels of SHBG were significantly increased in AD patients compared to
healthy controls (SHBG MD 12.94 nmol/l, 95%CI 2.68, 23.20). Conclusion: Patients with AD had higher plasma levels
of SHBG. The up-regulated levels of plasma SHBG show preliminary supportive evidence that SHBG and the bioavailability
of functional sex hormones in plasma may be linked to the pathogenesis of AD.
