Coenzyme Q10 and the exclusive club of diseases that show a limited response to treatment

被引:3
作者
Turton, Nadia [1 ]
Bowers, Nathan [1 ]
Khajeh, Sam [1 ]
Hargreaves, Iain P. [1 ]
Heaton, Robert A. [1 ]
机构
[1] Liverpool John Moores Univ, Sch Pharm & Biomol Sci, Liverpool, Merseyside, England
来源
EXPERT OPINION ON ORPHAN DRUGS | 2021年 / 9卷 / 05期
关键词
Coenzyme Q(10); mitochondrial electron transport chain disorders; multiple sclerosis; Parkinson's disease; EARLY PARKINSON-DISEASE; MULTIPLE-SCLEROSIS; OXIDATIVE STRESS; DOUBLE-BLIND; MITOCHONDRIAL DYSFUNCTION; RELATIVE BIOAVAILABILITY; CEREBROSPINAL-FLUID; TRIAL; BRAIN; SUPPLEMENTATION;
D O I
10.1080/21678707.2021.1932459
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Introduction: Coenzyme Q(10) (CoQ(10)) is a ubiquitous organic molecule with a significant role in the mitochondrial electron transport chain (ETC). As a result of its role in such an important biological process, (CoQ10) deficiency has been implicated in the pathogenesis of numerous diseases such as Parkinson's disease (PD) and multiple sclerosis (MS). This has led to multiple attempts to use CoQ(10) supplementation as a treatment or pre-treatment with varying degrees of success. Areas covered: The present review will identify evidence of mitochondrial dysfunction in MS, PD and mitochondrial ETC disorders. In addition, the inability of Co-10 supplementation to elicit significant clinical outcome in these disorders and possible flaws in these studies will be discussed. The databases utilized for this review were the Web of science and PubMed, with inclusive dates (1957-2021). Expert opinion: A lack of improved neurological outcome in these disorders post treatment with CoQ(10) may be attributable to the limited ability of CoQ(10) to cross the blood-brain barrier. Thus, CoQ(10) alternatives should also be considered. Other factors including time of disease diagnosis, dosage, administration, and duration of CoQ(10) therapy may have a significant influence on the efficacy of this treatment.
引用
收藏
页码:151 / 160
页数:10
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