Dataset Information

Aberrations in Oxidative Stress Markers in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis.

ABSTRACT: Oxidative stress has been reported to be involved in the onset and development of amyotrophic lateral sclerosis (ALS). Data from clinical studies have highlighted increased peripheral blood oxidative stress markers in patients with ALS, but results are inconsistent. Therefore, we quantitatively pooled data on levels of blood oxidative stress markers in ALS patients from the literature using a meta-analytic technique. A systematic search was performed on PubMed and Web of Science, and we included studies analyzing blood oxidative stress marker levels in patients with ALS and normal controls. We included 41 studies with 4,588 ALS patients and 6,344 control subjects, and 15 oxidative stress marker levels were subjected to random-effects meta-analysis. The results demonstrated that malondialdehyde (Hedges' g, 1.168; 95% CI, 0.812 to 1.523; P < 0.001), 8-hydroxyguanosine (Hedges' g, 2.194; 95% CI, 0.554 to 3.835; P = 0.009), and Advanced Oxidation Protein Product (Hedges' g, 0.555; 95% CI, 0.317 to 0.792; P < 0.001) levels were significantly increased in patients with ALS when compared with control subjects. Uric acid (Hedges' g, -0.798; 95% CI, -1.117 to -0.479; P < 0.001) and glutathione (Hedges' g, -1.636; 95% CI, -3.020 to -0.252; P = 0.02) levels were significantly reduced in ALS patients. In contrast, blood Cu, superoxide dismutase, glutathione peroxidase, ceruloplasmin, triglycerides, total cholesterol, low-density lipoprotein, high-density lipoprotein, coenzyme-Q10, and transferrin levels were not significantly different between cases and controls. Taken together, our results showed significantly increased blood levels of 8-hydroxyguanosine, malondialdehyde, and Advanced Oxidation Protein Product and decreased glutathione and uric acid levels in the peripheral blood of ALS patients. This meta-analysis helps to clarify the oxidative stress marker profile in ALS patients, supporting the hypothesis that oxidative stress is a central component underpinning ALS pathogenesis.

SUBMITTER: Wang Z

PROVIDER: S-EPMC6590548 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Aberrations in Oxidative Stress Markers in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis.

Wang Zihao Z Bai Zhile Z Qin Xiaoyan X Cheng Yong Y

Oxidative medicine and cellular longevity 20190609

Oxidative stress has been reported to be involved in the onset and development of amyotrophic lateral sclerosis (ALS). Data from clinical studies have highlighted increased peripheral blood oxidative stress markers in patients with ALS, but results are inconsistent. Therefore, we quantitatively pooled data on levels of blood oxidative stress markers in ALS patients from the literature using a meta-analytic technique. A systematic search was performed on PubMed and Web of Science, and we included ...[more]

PMID: 31281567

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Project description:Background: The effect of herbal medicine (HM) on amyotrophic lateral sclerosis (ALS) is controversial. Clinical trials investigating HMs continue; however, the use of HM is still questioned. We aimed to systematically review the literature pertaining to the effects and safety of HM in ALS. Methods: Randomised controlled trials (RCTs) that investigated the efficacy of HMs in ALS patients compared to any types of controls were identified. Nine databases and six registers were searched from their inception dates to 25 March 2022. Per the PRISMA guidelines, trials were identified and extracted. The risk of bias was evaluated using the Cochrane's tool. Certainty of evidence was assessed as per the GRADE criteria. Forest plots were constructed to assess the effect size and corresponding 95% CIs using fixed-effect models, and random-effect models were employed when required. The primary outcome was the activity limitation measured by validated tools, such as the revised ALS Functional Rating Scale. Results: Twenty studies (N = 1,218) were eligible. Of these, only five studies were double-blinded, and two were placebo-controlled. Fourteen HMs (fifty-one single botanicals) were involved; Astragalus mongholicus Bunge, Atractylodes macrocephala Koidz., and Glycyrrhiza glabra L. were commonly used in nine, eight, and six trials, respectively. For delaying activity limitation, Jiweiling injection (MD, 2.84; 95% CI, 1.21 to 4.46; p = 0.0006) and Shenmai injection (SMD, 1.07; 0.69 to 1.45; p < 0.00001) were significantly more efficacious than Riluzole, but the evidence was low quality. For ameliorating motor neuron loss, Jiweiling injection [right abductor pollicis brevis (APB): MD, 32.42; 7.91 to 56.93; p = 0.01 and left APB: MD, 34.44; 12.85 to 56.03; p = 0.002] was favoured, but the evidence was very low quality. Nine studies reported one hundred and twenty-three adverse events, twenty-six of which occurred in the treatment groups and ninety-seven in the control groups. Conclusion: Very low to low quality of evidence suggests that HMs seem to produce superior treatment responses for ALS without increased risk of adverse events. Additional studies with homogeneous participants, reduced methodological issues, and more efficient outcome measures are required to provide confirmatory evidence. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42021277443.

Project description:Interventions targeting mitochondrial dysfunction have the potential to extend survival in preclinical models of amyotrophic lateral sclerosis. The aim of this systematic review was to assess the efficacy of targeting mitochondria as a potential therapeutic target in amyotrophic lateral sclerosis. Preclinical studies written in the English language were identified with no restrictions on publication date from PubMed, Medline and EMBASE databases. All studies adopting interventions targeting mitochondria to treat amyotrophic lateral sclerosis in genetic or drug-induced organism models were considered for inclusion. A total of 76 studies were included in the analysis. Survival data were extracted, and the meta-analysis was completed in RevMan 5 software. We show that targeting mitochondrial dysfunction in amyotrophic lateral sclerosis results in a statistically significant improvement in survival (Z = 5.31; P<0.00001). The timing of administration of the intervention appears to affect the improvement in survival, with the greatest benefit occurring for interventions given prior to disease onset. Interventions at other time points were not significant, although this is likely to be secondary to a lack of publications examining these timepoints. The quality score had no impact on efficacy, and publication bias revealed an overestimation of the effect size, owing to one outlier study; excluding this led to the recalculated effect size changing from 5.31 to 3.31 (P<0.00001). The extant preclinical literature indicates that targeting mitochondrial dysfunction may prolong survival in amyotrophic lateral sclerosis, particularly if the intervention is administered early. A limitation of current research is a significant bias towards models based on superoxide dismutase 1, with uncertainty about generalisability to amyotrophic lateral sclerosis with an underlying TAR DNA binding protein 43 proteinopathy. However, further mechanistic research is clearly warranted in this field.

Dataset Information

Aberrations in Oxidative Stress Markers in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis.

Publications

Aberrations in Oxidative Stress Markers in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis.

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