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Lysophospholipids in the limelight: autotaxin takes center stage.

ABSTRACT: Lysophosphatidic acid (LPA) is a serum phospholipid that evokes growth factor-like responses in many cell types through the activation of its G protein-coupled receptors. Although much is known about LPA signaling, it has remained unclear where and how bioactive LPA is produced. Umezu-Goto et al. (2002)(this issue, page 227) have purified a serum lysophospholipase D that generates LPA from lysophosphatidylcholine and found it to be identical to autotaxin, a cell motility-stimulating ectophosphodiesterase implicated in tumor progression. This result is surprising, as there was previously no indication that autotaxin could act as a phospholipase.

SUBMITTER: Moolenaar WH

PROVIDER: S-EPMC2173118 | biostudies-other | 2002 Jul

REPOSITORIES: biostudies-other

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Project description:Bipolar Disorder (BD) is a major psychiatric illness affecting up to 5% of the population. BD can progress over time to a chronic "neuroprogressive" course with cognitive and functional impairment. Currently, there are no validated predictors indicating which patients will develop a neuroprogressive course and there are no specific treatments. This review presents data supporting a novel hypothesis on the mechanisms underlying bipolar neuroprogression. Insulin resistance (IR) is present in 52% of BD patients and is associated with chronic course, treatment nonresponse, adverse brain changes and cognitive impairment. Further, bipolar morbidity increases 12-fold following the onset of IR indicating that IR may modify disease progression. I review evidence that IR is a testable and treatable modifying factor in neuroprogression and that reversing IR may be an efficient (and perhaps the only) means of obtaining remission in some patients. I draw a parallel with Helicobacter pylori in peptic ulcer disease (a novel mechanism that brought together two previously unrelated phenomena that uncovered a new treatment approach). This model of bipolar progression combines shared dysregulated mechanisms between IR and BD, allowing for early screening, case finding, and monitoring for neuroprogression, with the potential for intervention that could prevent advanced bipolar illness. KEY MESSAGES Neuroprogression in bipolar disorder is defined by a more severe form of illness and poor outcome. Currently, there are no validated predictors of neuroprogression, which could help inform treatment and improve prognosis. Insulin resistance is present in more than half of all bipolar patients and is associated with a chronic course of illness, lack of response to mood stabilizing treatment, cognitive impairment and poor functional outcomes. Insulin resistance may modify the course of bipolar disorder and promote neuroprogression. Insulin resistance may be a testable and potentially modifiable risk factor for neuroprogression in bipolar disorder.

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Lysophospholipids in the limelight: autotaxin takes center stage.

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