Glucan synthase is not present in mammalian cells, so it is an attractive target for antifungal activity. Semisynthesis
Anidulafungin is manufactured via semi-synthesis. The starting material is echinocandin B (a lipopeptide fermentation product of Aspergillus nidulans or the closely related species, A. rugulosus), which undergoes deacylation (cleavage of the linoleoyl side chain) by the action of a deacylase enzyme from the bacterium Actinoplanes utahensis; in three subsequent synthetic steps, including a chemical reacylation, the antifungal drug anidulafungin is synthesized. History
Anidulafungin was originally discovered at Lilly laboratories by Turner and Debono and licensed to Vicuron Pharmaceuticals who submitted it to the FDA. Pfizer acquired the drug upon its acquisition of Vicuron in the fall of 2005. Pfizer gained approval by the Food and Drug Administration (FDA) on February 21, 2006. == References ==
Other MRI indicators of CAA include white matter hyperintensities and cortical thinning. Management
The aim in cerebral amyloid angiopathy is to treat the symptoms, as there is no current cure. Physical, occupational and/or speech therapy may be helpful in the management of this condition. History
Gustav Oppenheim was the first to report vascular amyloid β deposits on the vasculature of the central nervous system in 1909. The first paper focusing solely on what would come to be known as CAA was published in 1938 by WZ Scholz. In 1979, H. Okazaki published a paper implicating CAA in certain cases of lobar intracerebral hemorrhage. The Boston Criteria for CAA originated in a 1995 paper from Harvard Medical School. References
Further reading
Chao, Christine P.; Kotsenas, Amy L.; Broderick, Daniel F. (September 1, 2006). "Cerebral Amyloid Angiopathy: CT and MR Imaging Findings". RadioGraphics. 26 (5): 1517–1531. doi:10.1148/rg.265055090. ISSN 0271-5333. PMID 16973779. == External links ==