Increased oxidative stress in lymphocytes from untreated Parkinson's disease patients

Prigione, Alessandro; Isaias, Ioannis U.; Galbussera, Alessio; Brighina, Laura; Begni, Barbara; Andreoni, Simona; Pezzoli, Gianni; Antonini, Angelo; Ferrarese, Carlo

doi:10.1016/j.parkreldis.2008.05.013

Cited by 34 publications

(24 citation statements)

References 5 publications

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“…This suggests an antioxidant effect of l-dopa (11). Notably, increased oxidative stress was reported in lymphocytes from untreated patients with PD (12). It would be of interest to confirm our results with greater numbers of patients and in patients not treated pharmacologically.…”

supporting

confidence: 80%

Plasmalogens as a marker of elevated systemic oxidative stress in Parkinson's disease

Dragonas¹,

Bertsch

Sieber³

et al. 2009

Clinical Chemistry and Laboratory Medicine

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supporting

confidence: 80%

Plasmalogens as a marker of elevated systemic oxidative stress in Parkinson's disease

Dragonas¹,

Bertsch

Sieber³

et al. 2009

Clinical Chemistry and Laboratory Medicine

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“…Moreover, mitochondrial dysfunctions in aging and neurodegenerative disorders such as PD can be detected also in peripheral somatic cells [64][65][66]. Whether the pre-existing perturbation of mitochondrial functionality can be corrected upon iPSC generation is, thus, an essential question that needs to be addressed.…”

Section: Implications For the Use Of Human Ips Cells For In Vitro Modmentioning

confidence: 99%

The Senescence-Related Mitochondrial/Oxidative Stress Pathway is Repressed in Human Induced Pluripotent Stem Cells

et al. 2010

Self Cite

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The ability of stem cells to propagate indefinitely is believed to occur via the fine modulation of pathways commonly involved in cellular senescence, including the telomerase, the p53, and the mitochondrial/oxidative stress pathways. Induced pluripotent stem cells (iPSCs) are a novel stem cell population obtained from somatic cells through forced expression of a set of genes normally expressed in embryonic stem cells (ESCs). These reprogrammed cells acquire self-renewal properties and appear almost undistinguishable from ESCs in terms of morphology, gene expression, and differentiation potential. Accordingly, iPSCs exhibit alterations of the senescence-related telomerase and p53 signaling pathways. However, although treatments with antioxidants have been recently shown to enhance cellular reprogramming, detailed information regarding the state of the mitochondrial/oxidative stress pathway in iPSCs is still lacking. Mitochondria undergo specific changes during organismal development and aging. Thus, addressing whether somatic mitochondria within iPSCs acquire ESC-like features or retain the phenotype of the parental cell is an unanswered but relevant question. Herein, we demonstrate that somatic mitochondria within human iPSCs revert to an immature ESC-like state with respect to organelle morphology and distribution, expression of nuclear factors involved in mitochondrial biogenesis, content of mitochondrial DNA, intracellular ATP level, oxidative damage, and lactate generation. Upon differentiation, mitochondria within iPSCs and ESCs exhibited analogous maturation and anaerobic-to-aerobic metabolic modifications. Overall, the data highlight that human iPSCs and ESCs, although not identical, share similar mitochondrial properties and suggest that cellular reprogramming can modulate the mitochondrial/oxidative stress pathway, thus inducing a rejuvenated state capable of escaping cellular senescence.

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“…Oxidative stress may actively contribute to the decrease in lymphocytes observed in PD. Both whole cell and mitochondrial reactive oxygen species in PBMCs were found to be increased in PD patients [37]. …”

Section: Inflammatory and Immune Mechanisms Involved In Pdmentioning

confidence: 99%

Depression and Cognitive Impairment in Parkinson's Disease: A Role for Inflammation and Immunomodulation?

Rocha

Reis

Berghe

et al. 2014

Neuroimmunomodulation

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The etiology of Parkinson's disease (PD) is complex and not fully understood, most probably because of the multiplicity of factors involved. Inflammatory and abnormal immune responses have been hypothesized to play a crucial role in PD. Not only in the brain, but also peripherally, inflammation is believed to contribute to the onset and progression of the neurodegenerative process seen in PD. Furthermore, increased inflammatory responses have been described both in the brain and peripheral blood of PD subjects. Although PD is considered a motor disorder, nonmotor symptoms are extremely frequent and disabling. Cognitive impairment and mood alterations are such symptoms that deserve increased attention since on the one hand they can appear even before typical motor disturbances are recognized, and on the other hand they are associated with high morbidity and mortality. A growing body of evidence suggests the existence of a link between inflammatory-immune responses and the occurrence of depression and cognitive impairment in PD patients. However, not all data are equally conclusive and are sometimes even conflicting. The aim of this brief review is to give an overview of the possible role that inflammation and immunomodulation may play in PD together with their putative impact on mood and cognitive alterations. What clearly emerges from this work is the fact that studies performed until now lack standardized and comparable methods to analyze both clinical and biological parameters. It is thus difficult to conclusively link mood and cognitive changes to underlying pathological mechanisms. Additional studies in this direction are warranted to convincingly establish or refute any causative relation.

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Increased oxidative stress in lymphocytes from untreated Parkinson's disease patients

Cited by 34 publications

References 5 publications

Plasmalogens as a marker of elevated systemic oxidative stress in Parkinson's disease

Plasmalogens as a marker of elevated systemic oxidative stress in Parkinson's disease

The Senescence-Related Mitochondrial/Oxidative Stress Pathway is Repressed in Human Induced Pluripotent Stem Cells

Depression and Cognitive Impairment in Parkinson's Disease: A Role for Inflammation and Immunomodulation?

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