Decreased Number of Mitochondria in Leukoaraiosis.

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.

Evaluation of the MTHFR A1298C variant in leukoaraiosis.

Vascular demyelinization of the white matter of the brain is referred to as leukoaraiosis (LA). This very frequent entity is associated with a cognitive decline, thereby resulting in a deteriorating quality of life. Besides poorly controlled hypertension and aging, its development is reported to be associated with an elevated serum homocysteine level.

A homozygous genetic variant of mitochondrial uncoupling protein 4 affects the occurrence of leukoaraiosis.

Objectives: We hypothesized that an appropriate balance of the mitochondrial energy production is essential in the maintenance of the glia cells in the brain. The aim of this study was to examine the roles of the rs10807344 and rs2270450 genetic variants of mitochondrial uncoupling protein 4 in the development of vascular demyelinization of the white matter of the brain, referred to as leukoaraiosis (LA). The mUCPs are presumed to be of great importance in the regulation of the mitochondrial membrane potential (MMP) and the cellular energy metabolism.

Evaluation of the genetic variants of kinesin motor protein in ischemic stroke.

Background: The kinesin light-chain 1 genetic variants G56836C, A185C, and C406T were earlier found to amplify the development of leukoaraiosis in hypertensive smokers. These 3 variants were presumed to affect the function of the mitochondria, thereby giving rise to sensitivity to a chronic ischemic state. We have now extended our investigations to examine how the above genetic variants affect the occurrence of ischemic stroke.

A homozygous genetic variant of mitochondrial uncoupling protein 4 exerts protection against the occurrence of multiple sclerosis.

Multiple sclerosis (MS), which results in damage of the white matter at multiple foci, poses a far-reaching public health problem in view of the burden it imposes on the affected young and middle-aged. Some previous data suggested that roles could be played in the demyelinization of the white matter of the brain by the malfunctioning of the mitochondria and mitochondria-associated reactive oxygen species. In this context, we hypothesized that the finely tuned dynamic stability of the mitochondrial membrane potential (MMP), which is the main mirror of the functional state of the mitochondria, is essential for the intact nature of the glia cells in the brain.