MICRORNA-339-5P IS DYSREGULATED IN ALZHEIMER'S DISEASE AND IS INVERSELY PROPORTIONAL TO BACE1 EXPRESSION: IMPLICATION IN TESTING NOVEL DRUG TARGETS

vascular diameter. Yet, it is not clear, if these mechanisms to increase cerebral blood flow and sustenance can be found in both mice and men, if they are common within mouse models at all, or if there are probably misinterpretations of published data. Methods: Real comparative quantitative data between human AD cases and AD model mice are not available today. Thus we created a setup comparing CAA, vascular diameter and number in APP SLmodel mice at different ages and humanAD cases at different Braak stages of disease. CAA was immunohistochemically evaluated using a colabeling of an amyloid plaque marker (6E10) with Annexin-IV and smooth muscle actin to be able to directly quantify vascular amyloid load on arteries and venules. Results: CAA is related to arteries and does hardly appear at venules in both mice and men. APP SL mice react with an increased vascular diameter on amyloid load rather than with angiogenesis. Also in humans, no increase of the vessel number but rather an increase in vascular diameter of amyloid loaded vessels seems present. Furthermore, and as in mice over age, CAA increases with Braak stage in most cases.Conclusions: Obtained data support the thesis that, CAA is growing with age in APP SL mice and Braak stage in humans, and that the typical reaction to CAA is an increase of blood volume rather than an increase of arterial network. Differences and parallels between mice and men are presented and methodological topics discussed.