ArticleAnnals of translational medicine2015
Mitochondrial dysfunction in Kennedy's disease: a new pharmacological target?
Article in Annals of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed.
- Altered Metabolism in Motor Neuron Diseases: Mechanism and Potential Therapeutic Target.Cells · 2023Review
- Clinical manifestations and AR gene mutations in Kennedy's disease.Functional & integrative genomics · 2019Article
- Erratum to Mitochondrial dysfunction in Kennedy's disease: a new pharmacological target?Annals of translational medicine · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial impairment and elevated oxidative stress have been implicated in the pathogenesis of Kennedy's disease. However, there is still no study describing the mitochondrial nutrient management in patients with Kennedy's disease.
methodsWe assessed the clinical and electrophysiological features in a patient with Kennedy's disease. This patient was diagnosed by genetic analysis. We also measured the plasma 8-hydroxydeoxyguanosine (8-OHdG) levels of the patient and his family members using commercial enzyme-linked immunosorbent assay (ELISA). Treatment with intravenous L-carnitine (2 g/day) for the patient was started on admission, followed by two weeks.
resultsRoutine laboratory tests revealed a severe elevation of creatine kinase (CK) (606.5 U/L; normal value: 15-170 U/L). Sequencing of the first exon of androgen receptor (AR) revealed an increased number of CAG repeat (50; the normal range from 10-36) in the patient. Plasma 8-OHdG level in the patient was relatively elevated (34.68±1.01 ng/mL) compared with the female carriers and non-carriers. Two weeks after L-carnitine treatment, we observed a reduction of approximately 40% in CK level (391 U/L) in the patient.
conclusionsOxidative stress resulting from mitochondrial dysfunction could be involved in Kennedy's disease. Targeting the mitochondrial dysfunction in Kennedy's disease may have significant therapeutic potential.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.