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Modulation of O‐GlcNAc levels as a disease modifying approach for Alzheimer disease (223.3)
Author(s) -
Yuzwa Scott,
Shan Xiaoyang,
Hein Julia,
Cekic Nevena,
Jones Bryan,
Gong ChengXin,
Watson Neil,
Vocadlo David
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.223.3
Subject(s) - disease , neuroprotection , genetically modified mouse , alzheimer's disease , glycosylation , pathological , microbiology and biotechnology , cytoplasm , chemistry , neuroscience , biology , transgene , biochemistry , medicine , gene
Protein O‐glycosylation with N‐acetylglucosamine (O‐GlcNAc) is found in the nucleus and cytoplasm of multicellular eukaryotes. O‐GlcNAc is particularly abundant in brain tissue and is a glucose responsive post‐translational modification, which is interesting given that impaired glucose utilization is an early pathological feature occurring in the brains of Alzheimer patients. In this presentation I will discuss the generation of inhibitors that slow removal of O‐GlcNAc as well as the neuroprotective effects of such inhibitors in tissue culture as well as transgenic mouse models of Alzheimer disease.