Reduced noncovalent connections in leukoaraiosis

Abstract

Leukoaraiosis is manifested as diffuse areas of hypodensity on CT scans and as hyperintensity signals on T2-weighted MRI scans. This neuroimaging phenomenon is frequently associated with cognitive decline in the middle-aged or elderly. Ischemic demyelinization or chronic perivascular toxic edema in the white matter of the brain is presumed to be behind this entity. Genetic and environmental factors together lead to the development of leukoaraiosis. The possibility of hypoxia-induced cytoskeleton damage was suggested by recent experimental genetic data. This article discusses the chemical and biochemical consequences of this possibility. It suggests a new approach to leukoaraiosis by linking genetic data, medicinal chemistry, system theory and histopathological data. In accordance with this chemical model, a synchronously evolving slight intracellular ATP depletion along the glial cytoplasm may lead to an unstable biochemical condition in glial cells, which finally predisposes to leukoaraiosis.