At Mass General Hospital, Susanne Janneke van Veluw, gives an impressive explanation of the pathophysiology of microinfarts and microbleeds due to CAA. Microinfarts seem to come from blood vessels that retain amyloid-beta, lose smooth muscle cells, and therefore become stiff–possibly leading to an infart. Microbleeds seem to occur when cells lose both amyloid-beta and smooth muscle cells causing weakened cell walls. Experiments with Wild Type mice (WT and blue in the right-side diagram below) and CAA mice (Tg and pink in the diagram) show that, in mice with CAA, leakage from damaged blood vessels is cleared from the brain more slowly. This appears to be because WT mice –in this experiment — are capable of a maximum dilation of nearly 14% while the CAA mice can only achieve about an 8% dilation. Dr. van Veluw makes a strong case that the loss of smooth muscle cells is a key factor leading to reduced amyloid-beta clearance and therefore increased risk of microinfarts, microbleeds, or other CAA symptoms.
