Background And Aims: Leukoaraiosis (LA), one of the most frequent causes of an age-associated cognitive decline, can be associated with a poor quality of life, leading overall to far-reaching public health problems. Chronic hypoxia of the white matter of the brain may be a factor triggering this entity. LA may develop as a consequence of chronically insufficient cellular energy production and the accumulation of free radicals.
Methods: In this context, after hypothesizing that the number of healthy mitochondria can be crucial in this complex process, a case-control LA study was carried out in which we analyzed the numbers of deleted and non-deleted mitochondria (the common D-loop deletion) per white blood cell. A total of 234 patients with LA and 123 MRI alteration-free subjects served as a control group.
Results: Interestingly, it emerged that the ratio of deleted relative to non-deleted mitochondria is strongly associated with the risk of LA. The calculated K ratio in the LA group was significantly lower than the K ratio in the controls (LA: K 0.37 95% CI 0.05; controls: K 0.48, 95% CI 0.076, p < 0.001).
Conclusions: Our study suggests that the ratio of the dmDNA and mDNA can be of great importance in the pathogenesis of LA.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.arcmed.2015.11.002 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Decreased Number of Mitochondria in Leukoaraiosis.
Arch Med Res
November 2015
Department of Medical Microbiology and Immunology, Faculty of Medicine, University of Szeged, Szeged, Hungary.
Background And Aims: Leukoaraiosis (LA), one of the most frequent causes of an age-associated cognitive decline, can be associated with a poor quality of life, leading overall to far-reaching public health problems. Chronic hypoxia of the white matter of the brain may be a factor triggering this entity. LA may develop as a consequence of chronically insufficient cellular energy production and the accumulation of free radicals.
View Article and Find Full Text PDFIncreased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis.
Arch Immunol Ther Exp (Warsz)
December 2009
Department of Periodontology, Faculty of Dentistry, Ataturk University, Erzurum, Turkey.
Introduction: Oxidative stress may contribute to the pathogenesis of periodontitis. However, the detailed molecular mechanism remains unclear. Both 8-hydroxydeoxyguanosine (8-OHdG) and mitochondrial DNA (mtDNA) deletion have been reported as early oxidative DNA damage markers.
View Article and Find Full Text PDFAge-associated mitochondrial DNA deletions are not evident chronically after experimental brain injury in the rat.
J Neurotrauma
February 2003
Head Injury Center, Department of Neurosurgery, University of Pennsylvania, Philadelphia, PA 19104-6316, USA.
The enduring cognitive and sensorimotor deficits that result from traumatic brain injury (TBI) are associated with metabolic stress and free radical cascades, which establish conditions that may promote mitochondrial DNA (mtDNA) deletion and oxidation, often observed as a consequence of normal aging. Without substantial mtDNA repair mechanisms, permanent alterations to essential mitochondrial enzymes could perpetuate post-injury pathologic cascades. To determine whether mitochondria from the injured cortex and hippocampus sustain mtDNA damage after TBI, we evaluated mtDNA deletion and oxidation following lateral fluid percussion TBI in the anesthetized adult Sprague-Dawley rat (4 months) compared with uninjured adult and aged rats (n = 4/group).
View Article and Find Full Text PDFMultiple hepatic mitochondrial DNA deletions suggest premature oxidative aging in alcoholic patients.
J Hepatol
July 1997
INSERM Unité 24 and Centre de Recherche de Physiopathologie Hépatique(Association Claude Bernard), Hôpital Beaujon, Clichy, France.
Background/aims: A 4977-base pair deletion has been detected in the hepatic mitochondrial DNA of alcoholic patients with microvesicular steatosis, a lesion ascribed to impaired mitochondrial beta-oxidation. However, only a single deletion had been looked for in this previous study, and it could not be determined whether the deletion was preexisting or acquired. Alcohol abuse increases the formation of reactive oxygen species in hepatic mitochondria.
View Article and Find Full Text PDFHepatic mitochondrial DNA deletion in alcoholics: association with microvesicular steatosis.
Gastroenterology
January 1995
INSERM Unité 24, Hôpital Beaujon, Clichy, France.
Background/aims: Alcohol abuse may lead to microvesicular steatosis, a lesion ascribed to impaired mitochondrial function. Because alcohol abuse leads to reactive oxygen species in the hepatic mitochondria, it may damage mitochondrial DNA. The aim of this study was to look for the presence of the "common" 4977-base pair deletion in the hepatic mitochondrial DNA of alcoholic patients and age-matched, nonalcoholic controls.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!