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Research Article

Decreased Level of Serum Autoantibody Against LG72 is a Biosignature of Amyotrophic Lateral Sclerosis

, , , &
Pages 73-79 | Published online: 17 Dec 2015
 

Abstract

Aim

LG72 can increase mitochondrial ROSs and oxidative stress has been implicated in the pathophysiology of amyotrophic lateral sclerosis (ALS). The serum level of LG72 or LG72-related molecules might therefore be associated with ALS. Here, we aim to determine the serum autoantibody against LG72 has potential as a biomarker for the diagnosis of ALS.

Materials

Seventy-eighty patients with ALS, 45 patients with AD, 43 patients with PD and 88 healthy adults were enrolled.

Results

The concentration of serum autoantibody against LG72 was more than fourfold lower in ALS than other control groups (p < 0.001). The AUC was 0.9627 when the cut-off value for autoantibody concentration was 0.167 μg/ml.

Conclusion

This finding suggests that the autoantibody against LG72 might serve as a surrogate biomarker for ALS.

Financial & competing interests disclosure

This work was supported by a grant from the Ministry of Science and Technology of Taiwan (NSC102–2628-B-039–008-MY3, MOST104-2632-B-039-002 and CMU104-S-15-04 to H-T Chang). This study is supported in part by Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW104-TDU-B-212–113002). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Ethical conduct of research

The authors state that they have obtained appropriate institutional review board approval or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations. In addition, for investigations involving human subjects, informed consent has been obtained from the participants involved.

Additional information

Funding

This work was supported by a grant from the Ministry of Science and Technology of Taiwan (NSC102–2628-B-039–008-MY3, MOST104-2632-B-039-002 and CMU104-S-15-04 to H-T Chang). This study is supported in part by Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW104-TDU-B-212–113002). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

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