Highlights
- •AD patients had higher hepcidin values than MCI and normal controls.
- •The TIBC was significantly lower in the AD group than MCI and normal controls.
- •Serum iron levels were lower in the AD group than controls.
- •Hepcidin levels were statistically significantly correlated with the CDR.
Abstract
Objectives
There are no generally accepted serum biomarkers for Alzheimer's disease (AD). We
investigated the clinical usefulness of measuring the serum hepcidin levels and iron
profile in patients with AD.
Materials & methods
The iron profile and hepcidin levels were measured in patients with AD (N = 70), minimal cognitive impairment (MCI, N = 39), and vascular dementia (VD, N = 25) and normal controls (N = 124). General cognitive tests were performed, and the relationships between cognition
and hepcidin levels or the iron profile were assessed.
Results
Patients with AD had higher hepcidin values than those with MCI and VD and normal
controls (median value: 39.00 vs. 30.81, 32.52, and 5.51 ng/ml, respectively, P < 0.001), and these differences were found in both men and women. The total iron-binding
capacity was significantly lower in the AD group than in any other groups (308.0 vs.
332.0, 329.0, and 330.5 μg/dl, respectively, P = 0.018), and serum iron levels were lower in the AD group than controls (79.1 vs.
107.2 μg/dl, P = 0.007). Hepcidin levels were statistically significantly correlated with the clinical
dementia rating (CDR, P = 0.040) with a Pearson's correlation coefficient of 0.253, and the patients with
AD with a CDR value >1 had significantly higher hepcidin values than those with a
CDR value of 1 (65.26 vs. 23.49 ng/ml, P = 0.020).
Conclusion
The measurement of serum hepcidin levels and the iron profile in patients with early
manifestations of cognitive functional loss might aid in the diagnosis of AD and the
assessment of disease severity when combined with other diagnostic parameters.
Keywords
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Article info
Publication history
Published online: June 10, 2019
Accepted:
June 9,
2019
Received in revised form:
June 6,
2019
Received:
January 16,
2019
Identification
Copyright
© 2019 Published by Elsevier B.V.
