Abstract
Huntington's disease (HD) is a hereditary autosomal dominant neurodegenerative disease. Although studies have shown that blood oxidative stress markers are dysregulated in HD patients, clinical data on the blood oxidative stress markers of HD patients is inconsistent. To better understand the pathogenesis of HD, we performed a systematic review and meta-analysis of blood oxidative stress markers in HD patients and healthy control (HC) subjects. A database search from PubMed and Web of Science identified 12 studies with 375 HD patients and 447 HC subjects in this meta-analysis. A random-effects meta-analysis showed that blood lipid peroxidation products (Hedges' g = 0.883, 95%CI = 0.637 to 1.130, p < 0.001), 8-hydroxyguanosine (Hedges' g = 1.727, 95%CI = 0.489 to 2.965, p = 0.006) levels, and the activity of glutathione peroxidase (Hedges' g = 2.026, 95%CI = 0.570 to 3.482, p = 0.006) were significantly increased in HD patients compared to controls. In contrast, reduced glutathione levels were lower in HD patients than in controls (Hedges' g = −0.611, 95%CI = −1.016 to − 0.207, p = 0.003). However, blood superoxide dismutase, cholesterol, high-density lipoproteins, low-density lipoproteins, and triglycerides did not show significant differences between cases and controls. Taken together, this study clarified the associations between blood oxidative stress markers and HD, supporting the clinical evidence that HD is accompanied by increased oxidative stress.
Highlights
Huntington’s disease (HD), known as Huntington’s chorea, is a hereditary, autosomal, and dominant neurodegenerative disease; the disease is caused by a dominantly inherited cytosine-adenine-guanine (CAG) trinucleotide repeat expansion in the huntingtin gene, on chromosome IV [1, 2]
We conducted a meta-analysis of these six studies and observed a significant increase in Lipid peroxidation product (LPO) levels in the HD patients compared to their respective controls (Figure 2(a); Hedges’ g = 0:883, 95%CI = 0:637 to 1:130, p < 0:001)
We performed subgroup analyses, and the results showed that LPO levels were significantly increased in both the erythrocytes (Figure S1; Hedges’ g = 0:768, 95%CI = 0:311 to 1:226, p = 0:001) and plasma (Figure S1; Hedges’ g = 0:930, 95%C I = 0:638 to 1:223, p < 0:001) from HD patients compared to their respective controls
Summary
Huntington’s disease (HD), known as Huntington’s chorea, is a hereditary, autosomal, and dominant neurodegenerative disease; the disease is caused by a dominantly inherited cytosine-adenine-guanine (CAG) trinucleotide repeat expansion in the huntingtin gene, on chromosome IV [1, 2]. There is no effective treatment for this devastating disease, and it is a burden to society, for affected individuals, and their families. It is important to better understand the pathophysiology of HD, and subsequently develop an effective treatment for the disease. Increasing evidence suggests that oxidative stress is a primary event in the neuropathology of neurodegenerative diseases [6, 7]. Oxidative stress can be defined as an imbalance between oxidants and antioxidants, in favor of oxidants, resulting in cell damage, dysfunction, or death. Previous studies have reported that blood oxidative stress markers were dysregulated in patients with neurodegenerative diseases, and that the related markers had the potential to inform the diagnosis of these diseases. The clinical data from these studies were largely inconsistent.
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