Affiliations: [a] National Institute of Mental Health, Klecany, Czech Republic | [b] Memory Disorders Clinic, Department of Neurology, 2nd Faculty of Medicine, Charles University in Prague and Motol University Hospital, Prague 5, Czech Republic | [c] International Clinical Research Center, St. Anne’s University Hospital Brno, Brno, Czech Republic | [d] Institute of Computer Science, Academy of Sciences, Praha 8, Czech Republic
Correspondence:
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Correspondence to: Zdena Kristofikova, Alzheimer Disease Center, National Institute of Mental Health, Topolova 748, 250 67 Klecany, Czech Republic. Tel.: +420 283 088 111; [email protected]
Abstract:
Background: Overexpression of the mitochondrial enzyme 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10, which is also known as the intracellular amyloid-β peptide (Aβ) binding protein) is observed in cortical or hippocampal regions of patients with Alzheimer’s disease (AD). It appears that 17β-HSD10 may play a role in the pathogenesis of AD.
Objective: We investigated the possibility that levels of 17β-HSD10 in cerebrospinal fluid could be a prospective biomarker of AD.
Methods: We estimated the enzyme levels in 161 people (15 non-demented controls, 52 people with mild cognitive impairment (MCI), 35 people with probable AD, or 59 people with other types of dementia) and compared them with those of Aβ1 - 42, tau, and phospho-tau.
Results: We found significantly higher levels of 17β-HSD10 in people with MCI due to AD (to 109.9% ), with AD (to 120.0% ), or with other types of dementia (to 110.9% ) when compared to the control group. The sensitivity of the new biomarker to AD was 80.0% , and the specificity was 73.3% (compared to controls) or 52.5–59.1% (compared to other types of dementia). Results of multiple linear regression and of correlation analysis revealed AD-mediated changes in links between 17β-HSD10 and Mini Mental State Examination score.
Conclusion: It seems that changes in 17β-HSD10 start many years before symptom onset, analogous to those in Aβ1 - 42, tau, or phospho-tau and that the levels are a relatively highly sensitive but unfortunately less specific biomarker of AD. A role of 17β-HSD10 overexpression in AD is discussed.
