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Lipid Classes and Fatty Acid Patterns are Altered in the Brain of γ‐Synuclein Null Mutant Mice
Author(s) -
Guschina Irina,
Millership Steve,
O’Donnell Valerie,
Ninkitalia,
Harwood John,
Buchman Vladimir
Publication year - 2011
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-010-3486-0
Subject(s) - phosphatidylethanolamine , synuclein , lipid metabolism , biology , phosphatidylserine , fatty acid , docosahexaenoic acid , clinical chemistry , biochemistry , medicine , endocrinology , neurochemistry , alpha synuclein , microbiology and biotechnology , phospholipid , phosphatidylcholine , neuroscience , polyunsaturated fatty acid , parkinson's disease , neurology , disease , membrane
The well‐documented link between α‐synuclein and the pathology of common human neurodegenerative diseases has increased attention to the synuclein protein family. The involvement of α‐synuclein in lipid metabolism in both normal and diseased nervous system has been shown by many research groups. However, the possible involvement of γ‐synuclein, a closely‐related member of the synuclein family, in these processes has hardly been addressed. In this study, the effect of γ‐synuclein deficiency on the lipid composition and fatty acid patterns of individual lipids from two brain regions has been studied using a mouse model. The level of phosphatidylserine (PtdSer) was increased in the midbrain whereas no changes in the relative proportions of membrane polar lipids were observed in the cortex of γ‐synuclein‐deficient compared to wild‐type (WT) mice. In addition, higher levels of docosahexaenoic acid were found in PtdSer and phosphatidylethanolamine (PtdEtn) from the cerebral cortex of γ‐synuclein null mutant mice. These findings show that γ‐synuclein deficiency leads to alterations in the lipid profile in brain tissues and suggest that this protein, like α‐synuclein, might affect neuronal function via modulation of lipid metabolism.