ArticleNeurogenetics2011
Shorter telomeres in patients with cerebral autosomal dominant arteriopathy and leukoencephalopathy (CADASIL).
Article in Neurogenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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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.
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Who cites it
5 citing papers in PubMed.
- Telomere length as a biomarker for cerebrovascular diseases: current evidence.Molecular biology reports · 2024Review
- ER stress induced immunopathology involving complement in CADASIL: implications for therapeutics.Acta neuropathologica communications · 2023Article
- Can telomere shortening in human peripheral blood leukocytes serve as a disease biomarker of Friedreich's ataxia?Antioxidants & redox signaling · 2013Article
- Telomere shortening and Alzheimer's disease.Neuromolecular medicine · 2013Review
- Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CADASIL is a hereditary systemic vasculopathy which affects mainly small cerebral arteries and is caused by mutations in the Notch3 gene. Misfolding of Notch3 is linked to endoplasmic reticulum stress and increased reactive oxygen species, which may result in dysfunction of endothelial cells, inflammation and ischemia. Oxidative stress and inflammation may induce a rapid telomere shortening in peripheral blood leukocytes (PBLs). The aim of this study was to assess the telomere length in PBLs from 29 patients with a genetic diagnosis of CADASIL by using a modified quantitative real-time polymerase chain reaction based assay. PBL telomere length was significantly shorter in CADASIL patients (T/S ratio = 0.17, 95% CI, 0.14-0.20) than in the controls (T/S ratio = 0.31, 95% CI, 0.27-0.35, t-test p < 0.001). Moreover, patients with functional dependence displayed shorter telomeres than those with functional independence (p = 0.039). Our data provide the first evidence that PBL telomere length is shortened in CADASIL disease, and this may be a systemic oxidative stress indicator in CADASIL patients, providing a possible biomarker of disease progression and for future therapeutic strategies.
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