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P4–024: Involvement of 5lipoxygenase in Alzheimer's disease tau neuropathology
Author(s) -
Pratico Domenico,
Golde Todd,
Chu Jin
Publication year - 2013
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.2013.05.1412
Subject(s) - phosphorylation , neuropathology , kinase , tau protein , endogeny , epitope , downregulation and upregulation , microbiology and biotechnology , chemistry , cyclin dependent kinase 5 , amyloid beta , synaptophysin , biology , neuroscience , alzheimer's disease , protein kinase a , medicine , cyclin dependent kinase 2 , biochemistry , antibody , immunohistochemistry , peptide , immunology , disease , gene
galactosylceramide was also observed, reaching statistical significance in the hippocampus of Braak III/IV subjects (P<0.05), and frontal cortex at stage V/VI (P<0.01). Conclusions: This is the first report describing loss of S1P, as well as galactosylceramide, in pre-clinical AD pathogenesis. In addition to its neuroprotective properties, S1P regulates glutamate secretion and long term potentiation in the hippocampus, and is consequently important in establishing spatial memory in mice (T. Kanno, et al, Neuroscience, 2010, 171:973-80). Loss of galactosylceramide in mice destabilizes myelin, causing defecits in neuronal conductivity (T. Coetzee, et al, Cell, 1996, 86:209-19). Future studies will investigate how loss of these lipids contributes to neurodegeneration in AD.