Increased Mitochondrial DNA Deletions in Substantia Nigra Dopamine Neurons of the Aged Rat

Parkinson, Gemma M.; Dayas, Christopher V.; Dw, Smith

doi:10.2174/1874609808666150122150850

Cited by 21 publications

(26 citation statements)

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“…Studies on animals gave quite similar results, i.e. accumulation of deletions in mtDNA in brains, particularly in substantia nigra, of PD models (Dolle et al, 2016;Parkinson et al, 2014;Tzoulis et al, 2016). Moreover, depletion of mtDNA was also reported in this disease (Grunewald et al, 2016).…”

Section: Mitochondrial Dysfunction and Oxidative Stress In Age Relatesupporting

confidence: 52%

Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases

Giorgi

Marchi

Simões

et al. 2018

International Review of Cell and Molecular Biology

284

162

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Aging has been linked to several degenerative processes that, through the accumulation of molecular and cellular damage, can progressively lead to cell dysfunction and organ failure. Human aging is linked with a higher risk for individuals to develop cancer, neurodegenerative, cardiovascular, and metabolic disorders. The understanding of the molecular basis of aging and associated diseases has been one major challenge of scientific research over the last decades. Mitochondria, the center of oxidative metabolism and principal site of reactive oxygen species (ROS) production, are crucial both in health and in pathogenesis of many diseases. Redox signaling is important for the modulation of cell functions and several studies indicate a dual role for ROS in cell physiology. In fact, high concentrations of ROS are pathogenic and can cause severe damage to cell and organelle membranes, DNA, and proteins. On the other hand, moderate amounts of ROS are essential for the maintenance of several biological processes, including gene expression. In this review, we provide an update regarding the key roles of ROS-mitochondria cross talk in different fundamental physiological or pathological situations accompanying aging and highlighting that mitochondrial ROS may be a decisive target in clinical practice.

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Section: Mitochondrial Dysfunction and Oxidative Stress In Age Relatesupporting

confidence: 52%

Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases

Giorgi

Marchi

Simões

et al. 2018

International Review of Cell and Molecular Biology

284

162

View full text Add to dashboard Cite

show abstract

“…These relatively high levels (40-60%) of mtDNA deletions were associated with a cytochrome c oxidase (COX) deficiency in individual neurons [22,24]. These studies have been confirmed and extended to rodent models [100][101][102]. It was reported that mtDNA levels are also decreased in PD [103].…”

Section: Parkinson's Diseasementioning

confidence: 96%

Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease

2018

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Mitochondria are essential organelles within the cell where most ATP is produced through oxidative phosphorylation (OXPHOS). A subset of the genes needed for this process are encoded by the mitochondrial DNA (mtDNA). One consequence of OXPHOS is the production of mitochondrial reactive oxygen species (ROS), whose role in mediating cellular damage, particularly in damaging mtDNA during ageing, has been controversial. There are subsets of neurons that appear to be more sensitive to ROS-induced damage, and mitochondrial dysfunction has been associated with several neurodegenerative disorders. In this review, we will discuss the current knowledge in the field of mtDNA and neurodegeneration, the debate about ROS as a pathological or beneficial contributor to neuronal function, bona fide mtDNA diseases, and insights from mouse models of mtDNA defects affecting the central nervous system.

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“…The age-related increase in mtDNA damage was shown in patients with sporadic Parkinson's disease [271]. Greater accumulation of mtDNA deletions was detected in the dopaminergic neurons of substantia nigra in old rats compared to young ones [272]. …”

Section: Oxidative Dna Damagementioning

confidence: 99%

Mitochondrial dysfunction and oxidative stress in aging and cancer

et al. 2016

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Aging and cancer are the most important issues to research. The population in the world is growing older, and the incidence of cancer increases with age. There is no doubt about the linkage between aging and cancer. However, the molecular mechanisms underlying this association are still unknown. Several lines of evidence suggest that the oxidative stress as a cause and/or consequence of the mitochondrial dysfunction is one of the main drivers of these processes. Increasing ROS levels and products of the oxidative stress, which occur in aging and age-related disorders, were also found in cancer. This review focuses on the similarities between ageing-associated and cancer-associated oxidative stress and mitochondrial dysfunction as their common phenotype.

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Increased Mitochondrial DNA Deletions in Substantia Nigra Dopamine Neurons of the Aged Rat

Cited by 21 publications

References 0 publications

Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases

Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases

Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease

Mitochondrial dysfunction and oxidative stress in aging and cancer

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