Published online Oct 26, 2013. doi: 10.4330/wjc.v5.i10.394
Revised: September 20, 2013
Accepted: October 11, 2013
Published online: October 26, 2013
Processing time: 129 Days and 10.6 Hours
The important role of atherosclerosis in pathophysiology of Alzheimer’s Disease has become evident. Mechanisms such as hyperlipidemia, inflammation, abdominal obesity and insulin resistance are important yet they may not fully explain the specific involvement of the Circle of Willis in these pathologies. The Circle of Wills is a complex geometrical structure which has several areas with different curvature as well as various branching angles of vessels composing the circle. The hemodynamics in this region should take into account the Dean number which indicates the influence of curvature on the resistance to blood flow. Thus, areas with various curvature and angles may have different hemodynamics and there are certain areas in the Circle of Willis that are more likely to develop atherosclerotic changes. Therefore, this could suggest the novel pathophysiological pathway resulting from the geometric peculiarities of the Circle of Willis. One of the directions of future research is to examine whether specific areas of the Circle of Willis are more likely to develop atherosclerotic changes compared to other ones. Selective areas of the Circle of Willis affected by atherosclerotic changes could indicate the primary role of atherosclerosis promoting Alzheimer’s disease although other pathophysiological mechanisms suggesting the opposite direction should be also examined in prospective studies.
Core tip: The Dean number can become an important local pathophysiological mechanism that can help to explain the specific involvement of the Circle of Willis in atherosclerosis and Alzheimer’s Disease as anatomically different parts of the Circle of Willis would exhibit various degree of the curvature which would predispose to Alzheimer’s disease. This could possibly explain some sporadic cases of Alzheimer’s disease in the presence of minimal damage from atherosclerosis as well as open up new avenues for prevention of sporadic Alzheimer’s disease.