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• W2023841079 abstract "Frontotemporal dementia (FTD) is the second most common form of presenile dementia after Alzheimer's disease. In 2006, mutations were identified in the progranulin gene (GRN) that cause a common type of familial FTD associated with a specific pattern of protein aggregation in the brain (formerly FTLD-U, now FTLD-TDP). All of the disease-causing GRN mutations result in significantly decreased levels of progranulin protein. We are developing a mouse model of human progranulin insufficiency by producing mice that lack the gene that makes progranulin. The development of such a model will be crucial for future studies examining how the loss of progranulin causes the dysfunction and death of neurons in FTD. We aim to characterize the phenotype of mice with both conditional and constitutive deletion of the mouse progranulin gene (grn). We created conditionally-targeted grn mice. These mice were generated with a second-generation gene-trap targeting vector that features Flp recombinase sites flanking a lacZ/neomycin βgeo fusion protein cassette - comprising a consensus splice acceptor, an internal ribosome entry site preceding the βgeo coding sequence, and a polyadenylation signal following the stop codon such that it will be spliced downstream of grn exons 1-4. The β-galactosidase reporter gene is expressed under the native grn promoter and was used to assess grn expression in vivo. Integration of our gene-trap vector generated two independent mouse lines with a null allele of the grn gene. We have characterized the cellular and subcellular localization of progranulin in the developing and adult mouse CNS using both immunocytochemistry and β-galactosidase reporter expression in our grn-targeted mice. We will also present our behavioral, electrophysiologic and neuropathologic characterization of aged grn-deficient mice. Constitutively and conditionally-targeted grn mice will allow us to dissect the role of progranulin in distinct cell types and at defined times during development, and ultimately help enable us to understand how loss of progranulin function leads to CNS disease." @default.
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• W2023841079 date "2010-07-01" @default.
• W2023841079 modified "2023-09-27" @default.
• W2023841079 title "S1-02-03: Generation and characterization of a mouse model of progranulin deficiency" @default.
• W2023841079 doi "https://doi.org/10.1016/j.jalz.2010.05.190" @default.
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