| Abstract No.: | B-C2119 |
| Country: | Canada |
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| Title: | IDENTIFICATION OF GLYCEROPHOSPHOCHOLINE LIPID SPECIES ASSOCIATED WITH ALZHEIMER'S DISEASE |
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| Authors/Affiliations: | 1 Leigh Anne Swayne*; 1 Shawn Whitehead; 1 Weimin Hou; 1 Daniel Figeys; 1 Steffany Bennett;
1 University of Ottawa, ON, Canada
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| Content: | Objectives: Abnormal structural glycerophospholipid metabolism in neural cell membranes is a well-known pathological characteristic of Alzheimer’s disease (AD). Increased glycerophosphocholine and glycerophosphoethanolamine concentrations in brain and cerebrospinal fluid have been linked to accelerated cognitive decline in AD. Until recently, mechanistic insight into lipid changes has been hindered by the technical problems associated with identification and quantification of individual species within several thousand present in neural lipid extracts. The study of glycerophospholipid changes in AD have been restricted to “macro” analyses of subclasses, as defined by polar head groups (e.g. phosphocholine, phosphoethanolamine, phosphoserine) total number of carbons, and/or linkage to the glycerol backbone. New advances in mass spectrometry have significantly enhanced our capacity to resolve molecular subspecies. Here we sought to specifically identify possible novel glycerophosphocholine isoforms generated in human AD by employing these novel techniques.
Methods: We extracted glycerophospholipids from human control and AD temporal cortex using a modified Bligh/Dyer procedure, and performed nanoflow high-performance liquid chromatography electrospray ionization tandem mass spectrometry with precursor ion scan for phosphocholine. Using a similar protocol, we recently described marked changes in two predominant platelet activating factor PAF species (C16:0, C18:0), an abundant subclass of neural glycerophosphocholine species, over the course of PC12 cell differentiation (Whitehead et al. Anal Chem. 2007, 79:8539-48).
Results & Conclusions: Here we specifically identify several glycerophosphocholine species upregulated in Alzheimer’s disease neural tissue, and present a comprehensive glycerophosphocholine lipidome of human temporal cortex.
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