Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 34, Issue 1, Pages 148-157Publisher
KARGER
DOI: 10.1159/000362991
Keywords
Sphingosine-1-phosphate; S1P-Iyase; Neurodegeneration; Amyloid beta; cis-4-methylsphingosine; FTY720 (fingolimod); Alzheimer's disease; Tau
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Funding
- Deutsche Forschungsgemeinschaft (DFG) [EC-118/6-1, WA1477/8-1]
- collaborative research center 645 [TP A7]
- clinical research group KF0177 [WA1477/4-2]
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Sphingosine-1-phosphate (S1P), an evolutionary conserved bioactive lipid, is essential for brain development, but might also exert detrimental effects in terminally differentiated post mitotic neurons. Its concentration in the brain is tightly regulated by specific kinases and phosphatases, and mainly by the S1P degrading enzyme, S1P-lyase (S1PL). The role of S1P in neurons was initially studied in primary cultures by using structural analogues. During the last 3 years generation of a S1PL deficient mouse model substantially promoted our knowledge on the functional role of S1P metabolism in the brain, and its potential relation to neurodegenerative diseases. However, our understanding of the molecular mechanisms that underlie the physiological and pathophysiological actions of S1P in neurons remains rather scarce. Copyright (C) 2014 S. Karger AG, Basel
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