La maladie de Parkinson au Canada (serveur d'exploration)

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8OHdG is not a biomarker for Huntington disease state or progression

Identifieur interne : 000E80 ( Main/Exploration ); précédent : 000E79; suivant : 000E81

8OHdG is not a biomarker for Huntington disease state or progression

Auteurs : Beth Borowsky ; John Warner ; Blair R. Leavitt ; Sarah J. Tabrizi ; Raymund A. C. Roos ; Alexandra Durr ; Chris Becker ; Cristina Sampaio ; Allan J. Tobin ; Howard Schulman

Source :

RBID : PMC:3716347

Abstract

Objective:

To evaluate plasma 8-hydroxy-deoxy-guanosine (8OHdG) levels as a potential biomarker of premanifest and early Huntington disease (HD).

Methods:

Personnel from 2 independent laboratories quantified 8OHdG in blinded longitudinal plasma samples taken 24 months apart from 160 TRACK-HD participants, as well as samples containing control plasma with added (“spiked”) 8OHdG. One laboratory used a liquid chromatography–electrochemical array (LCECA) assay, and the other used liquid chromatography–mass spectrometry (LCMS).

Results:

The LCMS assay was more accurate than the LCECA assay for measurements of “spiked” 8OHdG levels in plasma. Neither assay demonstrated cross-sectional differences in plasma 8OHdG among controls, premanifest HD, and early symptomatic HD. Similarly, neither assay showed longitudinal changes in any disease group over 24 months.

Conclusions:

Plasma concentration of 8OHdG is not a biomarker of disease state or progression in HD. We recommend that future putative biomarker studies use blinded sample analysis, standard curves, independent analytical methods, and strict quality control of sample collection and storage.


Url:
DOI: 10.1212/WNL.0b013e318293e1a1
PubMed: 23616162
PubMed Central: 3716347


Affiliations:


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<title>Objective:</title>
<p>To evaluate plasma 8-hydroxy-deoxy-guanosine (8OHdG) levels as a potential biomarker of premanifest and early Huntington disease (HD).</p>
</sec>
<sec>
<title>Methods:</title>
<p>Personnel from 2 independent laboratories quantified 8OHdG in blinded longitudinal plasma samples taken 24 months apart from 160 TRACK-HD participants, as well as samples containing control plasma with added (“spiked”) 8OHdG. One laboratory used a liquid chromatography–electrochemical array (LCECA) assay, and the other used liquid chromatography–mass spectrometry (LCMS).</p>
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<title>Results:</title>
<p>The LCMS assay was more accurate than the LCECA assay for measurements of “spiked” 8OHdG levels in plasma. Neither assay demonstrated cross-sectional differences in plasma 8OHdG among controls, premanifest HD, and early symptomatic HD. Similarly, neither assay showed longitudinal changes in any disease group over 24 months.</p>
</sec>
<sec>
<title>Conclusions:</title>
<p>Plasma concentration of 8OHdG is not a biomarker of disease state or progression in HD. We recommend that future putative biomarker studies use blinded sample analysis, standard curves, independent analytical methods, and strict quality control of sample collection and storage.</p>
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