Pathological Changes Of Cerebral Arterioles In The Cases Of Cerebral Amyloid Angiopathy

Purpose The study aims at the changes of diameters of vessels and expression of α-SM-Actin in some cerebral arterioles with different severity of Aβ deposit in the cases of Cerebral amyloid angiopathy (CAA).Method Examine 53 archived frontal lobes of aged brains with Gongo red and using an antibody against β-amyloid peptide and confine 10 cases of CAA. In each cases, select the first 10 arterioles with circular profiles with 30~100μm external diameter and 10 with 100~300μm external diameter. Classify them into four groups: unaffected vessels, mild , moderate and severe Aβ deposits. 100 selected arterioles in 5 persons without CAA are regarded as control group. compare internal diameters, sclerotic index (SI) of vessels and the expression of α-SM-Actin of different groups in the same external diameter range.Result For arterioles with 30~100μm external diameter, SI of vessels with mild and moderate Aβ deposits are higher than those of control group ,though the internal diameters of them are not different from control group. Conversely , the internal diameters of severely affected vessels are larger and SI are smaller than those of controlled. There is no difference between Unaffected vessels and control group. For the arterioles with 100~ 300μm external diameter,the results are similar, except that SI of moderate AB deposits are not larger significantly. In the cases of CAA, positive VSMCs for a-SM-Actin are mainly located at inner of media. PU value are smaller than control group correlatedly with severity of amyloidosis. And unaffected vessels had no changes on PU value.conclusion In the early stage of amyloid angiopathy , Aβ are first located at the basal lamina around smooth muscle cells. Thus the vessel walls become thicker and lumens become narrow, cerebral blood flow is reduced. Whereas during the advanced stage, Aβ gradually spread towards the VSMCs. As deposits increase in size the VSMCs may show degenerative features. Due to the loss of VSMCs and changes of components of extracellular matrix, walls become thinner and lumens become larger , the arterioles are fragile. For the toxicity of adjacent amyloid peptides, VSMCs have been degenerating forall the course of disease and become dead in the end.