Trial reportCNS drugs2015
Mechanisms of Antioxidant Induction with High-Dose N-Acetylcysteine in Childhood Cerebral Adrenoleukodystrophy.
Trial report in CNS drugs, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Bridging psychiatry and rare genetic diseases: a scoping review of therapeutic strategies and diagnostic delay paired with healthcare economic burden analysis.Orphanet journal of rare diseases · 2025Article
- N-acetylcysteine Pharmacology and Applications in Rare Diseases-Repurposing an Old Antioxidant.Antioxidants (Basel, Switzerland) · 2023Review
- Isoprostanoid Plasma Levels Are Relevant to Cerebral Adrenoleukodystrophy Disease.Life (Basel, Switzerland) · 2022Article
- The Role of Oxidative Stress and Inflammation in X-Link Adrenoleukodystrophy.Frontiers in nutrition · 2022Review
- Identifying Biological Signatures of N-Acetylcysteine for Non-Suicidal Self-Injury in Adolescents and Young Adults.Journal of psychiatry and brain science · 2021Article
- N-acetylcysteine Provides Cytoprotection in Murine Oligodendrocytes through Heme Oxygenase-1 Activity.Biomedicines · 2020Article
- 25-hydroxycholesterol contributes to cerebral inflammation of X-linked adrenoleukodystrophy through activation of the NLRP3 inflammasome.Nature communications · 2016Article
- ABC Transporter Subfamily D: Distinct Differences in Behavior between ABCD1-3 and ABCD4 in Subcellular Localization, Function, and Human Disease.BioMed research international · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChildhood cerebral adrenoleukodystrophy (CCALD), a progressive demyelinating disease affecting school-aged boys, causes death within a few years. Oxidative stress is an important contributing factor. N-acetylcysteine (NAC; 280 mg/kg/day) added as adjunctive therapy to reduced-intensity hematopoietic cell transplantation (HCT) improves survival in advanced cases. However, the mechanisms underlying the benefits of NAC are unclear.
objectiveThe aim of this study was to understand the mechanism of action of NAC in the setting of HCT in CCALD.
methodsImmunoassays were carried out to determine changes in heme oxygenase-1 (HO-1) and ferritin expression in plasma samples collected from boys with CCALD at three different timepoints during the course of transplantation. In addition, the induction of HO-1 was also confirmed in normal fibroblasts following incubation with 10-100 µmol/L NAC for 4 h.
resultsFollowing NAC therapy we observed an increase in expression of the antioxidants HO-1 (~4-fold) and its effector ferritin (~160-fold) in patient samples as compared with baseline. We also observed that NAC exposure significantly increased HO-1 expression in fibroblasts.
conclusionOur data suggest that HO-1 is a possible target protein of NAC and a mediator of its cytoprotective effects in these patients.
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