Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways
Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways
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Author / Creator
Ibanez, Kristen R. , McFarland, Karen N. , Phillips, Jennifer , Allen, Mariet , Lessard, Christian B. , Zobel, Lillian , De La Cruz, Elsa Gonzalez , Shah, Shivani , Vo, Quan , Wang, Xue , Quicksall, Zachary , Ryu, Daniel , Funk, Cory , Ertekin-Taner, Nilüfer , Prokop, Stefan , Golde, Todd E. and Chakrabarty, Paramita
Publisher
England: BioMed Central
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Language
English
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Publisher
England: BioMed Central
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Contents
The S209F variant of Abelson Interactor Protein 3 (ABI3) increases risk for Alzheimer's disease (AD), but little is known about its function in relation to AD pathogenesis.
Here, we use a mouse model that is deficient in Abi3 locus to study how the loss of function of Abi3 impacts two cardinal neuropathological hallmarks of AD-amyloid β plaques...
Alternative Titles
Full title
Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways
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TN_cdi_doaj_primary_oai_doaj_org_article_38aa23abced645f493a2c58c36ef5035
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_38aa23abced645f493a2c58c36ef5035
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ISSN
1758-9193
E-ISSN
1758-9193
DOI
10.1186/s13195-022-01044-1
