Vascular Dementia

Biography

Biography: Hans Von Holst

Abstract

Increased intracellular water content defined as cytotoxic brain tissue edema is a serious secondary clinical complication to traumatic brain injury (TBI) and stroke and without knowledge to the etiology. Recently a hypothesis to the nervous tissue edema was presented suggesting that external dynamic and internal mechanical static impact forces caused protein unfolding resulting in an increased brain tissue water content and what happens with the metabolism in the long run. The hypothesis was confirmed by computer simulation tests. In this laboratory study we further evaluated the hypothesis by using the mature protein laminin LN521 upon the effects of both dynamic as well as static impact forces, respectively. The treated laminin solutions were then analyzed with denatured electrophoresis and Electron Microscopy showing aggregation and fragmentation of the laminin structures. The present laboratory results confirm earlier hypothesis and computer simulation suggesting for the first time that dynamic impact force in an accident and increased mechanical static force in stroke unfold mature proteins having the potential to increase the intracellular water content defined as cytotoxic brain tissue edema. The clinical condition resembles the phenomenon when elasmobranchs including white sharks prevent their cells from too high hydrostatic pressure in the deep sea. Thus, the present laboratory study results and knowledge from marine physics may be considered to improve the clinical treatment and outcome of TBI and stroke patients. This opens up new perspectives how vascular dementia in TBI and Stroke should be looked upon when it come sto clinical treatment.