ALS Article #1 Notes

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Department
Biological Sciences
Course
BIOD65H3
Professor
Joanne Nash
Semester
Fall

Description
Activated protein C therapy slows ALSlike disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells Zhong et al 2009Intro y APCendogenous plasma serine proteaseanticoagulation and cytoprotection y SOD1destroys radicals150 mutations linked to ALSpresent damage in motor neurons microglia astrocytes microvessel endotheliumG93A G85RG37R study used SOD1 SOD1 SOD1 y PAR1GPCR cleaved by APCfunctionalexpressed in platelets endothelium certain neurons y EPCRAPC receptor found specifically in endothelial cellsits through the EPCR that APC is transported into the spinal cord ISF y Sp1transcirption factorregulates expression of genes involved in cell growth apoptosis differentiation and immune responses y Hypomorph mutation that causes partial loss of gene function1 APC treatment delivered after disease onset controls progression of ALSlike diseaseG93Ay ALSlinked mutant SOD1 mice put into one of the following groups saline WTAPC active 3K3AAPC active 5AAPC active S360AAPC inactive y Given a low dose 40 gkgd ip or high dose 100 gkgd ip of either saline or one of the APC analogs 7 days after disease onset y Inactive S360AAPCno significant effect on survival lifespan or disease duration y Active WTAPC 3K3AAPC 5AAPCsignificant increase in lifespan and disease duration compared to salinetreated controls when given either low or high dose y Clotting time of both S360AAPC and 5AAPCreduced similarly
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