[Neuroscience] DHEAS and Alzheimer's disease

James Michael Howard jmhoward at anthropogeny.com
Tue Apr 4 07:23:56 EST 2006

I first suggested that low DHEA (derived from DHEAS) may result in
Alzheimer's disease in 1985 (copyrighted).

Biomed Chromatogr. 2006 Apr 1; [Epub ahead of print]

Rapid column-switching liquid chromatography/mass spectrometric assay for
DHEA-sulfate in the plasma of patients with Alzheimer's disease.

Cho SH, Jung BH, Lee WY, Chung BC.

Bioanalysis and Biotransformation Research Center, KIST, Chengryang, Seoul,
130-605, Korea.

A simple and highly sensitive method for the quantification of
dehydroepiandrosterone-3-sulfate (DHEAS) in human plasma was developed.
DHEAS was directly determined in plasma using column-switching liquid
chromatography/mass spectrometry (LC-MS). The plasma was filtered with a
membrane filter. The filtrate was injected onto a pre-column without
further sample preparation such as extraction or derivatization. The
pre-column was washed with an aqueous solution to remove interference and
the analyte was eluted into a reversed-phase C(18) analytical column for
separation and detection using a column-switching valve. The calibration
range of DHEAS was 0.01-10 micromol/L, and the linearity of the method was
0.999. The limit of detection (LOD) at a signal-to-noise (S/N) ratio of 3
was 5 nmol/L. The accuracy and precision (%CV) were less than 10% in
within-day and day-to-day variations. To explore the relationship between
Alzheimer's disease and the DHEAS level in human plasma, the concentrations
of DHEAS in female patients with Alzheimer's disease (n = 20) and in normal
female subjects (n = 20) were measured. The level of DHEAS was
significantly decreased in the plasma of patients with Alzheimer's disease
(p < 0.0002) compared with that in normal subjects. From the results, we
concluded that our method is sufficiently sensitivity and reliability for
the quantification of DHEAS in clinical samples. Plasma DHEAS concentration
could be an important marker to understand the pathogenesis of Alzheimer's
disease. Copyright (c) 2006 John Wiley & Sons, Ltd.

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