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P3‐327: Therapeutic suppression of tau kinases in the CNS with antisense oligonucleotides
Author(s) -
Wancewicz Edward,
Kordasiewicz Holly,
Mazur Curt,
Bennett Frank,
Marco Giorgetti
Publication year - 2012
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.05.1551
Subject(s) - gene knockdown , cyclin dependent kinase 5 , kinase , hippocampus , chemistry , phosphorylation , messenger rna , microbiology and biotechnology , biology , pharmacology , neuroscience , apoptosis , biochemistry , protein kinase a , cyclin dependent kinase 2 , gene
to target pathogenic tau in 4-, 8-, and 18-month-old P301L tau transgenic mice, a model of AD and FTD, that have an onset of NFT pathology at 6 months of age. After up to 10 months of treatment, the degree of NFT pathology was determined by histological analysis. Results:All age groups, NFT pathology was significantly reduced in treated compared to non-immunized mice. Similarly, phosphorylation of tau at pathological sites was reduced. In addition, increased astrocytosis was found in the oldest treated group. Conclusions: Our data suggests that tau-targeted immunization slows the progression of NFT pathology in a mouse model of tau pathology.