Study of telomere length and different markers of oxidative stress in patients with Parkinson's disease

Watfa, Ghassan; Dragonas, Charalampos; Brosche, Thorolf; Dittrich, Ralf; Sieber, Cornel; Alecu, Cosmin; Bénétos, Athanase; Nzietchueng, Rosine

doi:10.1007/s12603-010-0275-7

Cited by 66 publications

(38 citation statements)

References 33 publications

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“…Eight primary studies were included in the meta-analysis for PD and telomere length (Degerman et al, 2014; Eerola et al, 2010; Guan et al, 2008; Hudson et al, 2011; Schurks et al, 2014; Wang et al, 2008; Watfa et al, 2011). One study was not included in the meta-analysis as TL data were not available and it was not possible to obtain the information from the corresponding author after multiple attempts (Maeda et al, 2012).…”

Section: Resultsmentioning

confidence: 99%

Telomere length in Parkinson's disease: A meta-analysis

Forero

González-Giraldo

López-Quintero

et al. 2016

Experimental Gerontology

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Parkinson’s disease (PD) is a common and severe movement disorder. Differences in telomere length (TL) have been reported as possible risk factors for several neuropsychiatric disorders, including PD. Results from published studies for TL in PD are inconsistent, highlighting the need for a meta-analysis. In the current work, a meta-analysis of published studies for TL in PD was carried out. PubMed, Web of Science and Google Scholar databases were used to identify relevant articles that reported TL in groups of PD patients and controls. A random-effects model was used for meta-analytical procedures. The meta-analysis included eight primary studies, derived from populations of European and Asian descent, and did not show a significant difference in TL between 956 PD patients and 1284 controls (p value: 0.246). Our results show that there is no consistent evidence of shorter telomeres in PD patients and suggest the importance of future studies on TL and PD that analyze other populations and also include assessment of TL from different brain regions.

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Section: Resultsmentioning

confidence: 99%

Telomere length in Parkinson's disease: A meta-analysis

Forero

González-Giraldo

López-Quintero

et al. 2016

Experimental Gerontology

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“…One study found an increase in protein carbonyls in PD leukocytes [71], while another found no difference when compared to controls [97]. No differences in protein carbonyls are found in PD plasma [98]; yet this may be related to the clinical stage, as a different study found that protein carbonyls increased in later PD stages [71].…”

Section: Oxidative Damage In Human Pdmentioning

confidence: 99%

Oxidative damage to macromolecules in human Parkinson disease and the rotenone model

Sanders

Greenamyre

2013

Free Radical Biology and Medicine

292

204

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Parkinson’s disease (PD), the most common neurodegenerative movement disorder, is associated with selective degeneration of nigrostriatal dopamine neurons. While the underlying mechanisms contributing to neurodegeneration in PD appear to be multifactorial, mitochondrial impairment and oxidative stress are widely considered to be central to many forms of the disease. Whether oxidative stress is a cause or consequence of dopaminergic death, there is substantial evidence for oxidative stress in both human PD patients and in animal models of PD, especially using rotenone, a complex I inhibitor. There are many indices of oxidative stress, but this review covers the recent evidence for oxidative damage to nucleic acids, lipids and proteins in both the brain and peripheral tissues in human PD and in the rotenone model. Limitations of the existing literature and future perspectives are discussed. Understanding how each particular macromolecule is damaged by oxidative stress and the interplay of secondary damage to other biomolecules may help design better targets for treatment of PD.

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“…Furthermore, it has been shown that reactivation of telomerase in old, advanced generation (G4) mice of an inducible-TERT knock in mouse model can reverse neurodegeneration phenotypes associated with the accelerated aging phenotype in those mice (Jaskelioff et al). Finally, individuals with short telomeres in peripheral blood mononuclear cells (PBMC) appear to be more prone to neurodegenerative disorders such as AD, PD and dementia (Grodstein et al, 2008; Guan et al, 2012; Hochstrasser et al, 2012; Honig et al, 2012; Honig et al, 2006; Jenkins et al, 2006; Kume et al, 2012; Maeda et al, 2012; Martin-Ruiz et al, 2006; Panossian et al, 2003; Thomas et al, 2008; von Zglinicki et al, 2000; Watfa et al, 2011). Considering that telomere length is thought to be proportional within individuals across different organs, these data support an association between telomere length and neurodegeneration.…”

Section: Introductionmentioning

confidence: 99%

Generating Late-Onset Human iPSC-Based Disease Models by Inducing Neuronal Age-Related Phenotypes through Telomerase Manipulation

2016

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SUMMARY Modeling late onset disorders such as Parkinson’s disease (PD) using iPSC technology remains a challenge as current differentiation protocols yield cells with the properties of fetal-stage cells. Here we tested whether it is possible to accelerate aging in vitro to trigger late onset disease phenotypes in an iPSC model of PD. In order to manipulate a factor that is involved in natural aging as well as in premature aging syndromes, we used telomere shortening as an age-inducing tool. We show that shortened telomeres result in age-associated as well as potentially disease-associated phenotypes in human pluripotent stem cell (hPSC) derived midbrain dopamine (mDA) neurons. Our approach provides proof of concept for the further validation of telomere shortening as an induced aging tool for late onset diseases modeling.

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Study of telomere length and different markers of oxidative stress in patients with Parkinson's disease

Abstract: In PD, TL is shorter in presence of high oxidative stress as measured by carbonyl protein levels. The absence of telomere attrition with age among patients with PD could reflect a telomere regulation by mechanisms other than age.

Cited by 66 publications

References 33 publications

Telomere length in Parkinson's disease: A meta-analysis

Telomere length in Parkinson's disease: A meta-analysis

Oxidative damage to macromolecules in human Parkinson disease and the rotenone model

Generating Late-Onset Human iPSC-Based Disease Models by Inducing Neuronal Age-Related Phenotypes through Telomerase Manipulation

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