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.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.