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Dysregulation of lysophosphatidic acids in multiple sclerosis and autoimmune encephalomyelitis

Overview of attention for article published in Acta Neuropathologica Communications, June 2017
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Title
Dysregulation of lysophosphatidic acids in multiple sclerosis and autoimmune encephalomyelitis
Published in
Acta Neuropathologica Communications, June 2017
DOI 10.1186/s40478-017-0446-4
Pubmed ID
Authors

K. Schmitz, R. Brunkhorst, N. de Bruin, C. A. Mayer, A. Häussler, N. Ferreiros, S. Schiffmann, M. J. Parnham, S. Tunaru, J. Chun, S. Offermanns, C. Foerch, K. Scholich, J. Vogt, S. Wicker, J. Lötsch, G. Geisslinger, I. Tegeder

Abstract

Bioactive lipids contribute to the pathophysiology of multiple sclerosis. Here, we show that lysophosphatidic acids (LPAs) are dysregulated in multiple sclerosis (MS) and are functionally relevant in this disease. LPAs and autotaxin, the major enzyme producing extracellular LPAs, were analyzed in serum and cerebrospinal fluid in a cross-sectional population of MS patients and were compared with respective data from mice in the experimental autoimmune encephalomyelitis (EAE) model, spontaneous EAE in TCR(1640) mice, and EAE in Lpar2 (-/-) mice. Serum LPAs were reduced in MS and EAE whereas spinal cord LPAs in TCR(1640) mice increased during the 'symptom-free' intervals, i.e. on resolution of inflammation during recovery hence possibly pointing to positive effects of brain LPAs during remyelination as suggested in previous studies. Peripheral LPAs mildly re-raised during relapses but further dropped in refractory relapses. The peripheral loss led to a redistribution of immune cells from the spleen to the spinal cord, suggesting defects of lymphocyte homing. In support, LPAR2 positive T-cells were reduced in EAE and the disease was intensified in Lpar2 deficient mice. Further, treatment with an LPAR2 agonist reduced clinical signs of relapsing-remitting EAE suggesting that the LPAR2 agonist partially compensated the endogenous loss of LPAs and implicating LPA signaling as a novel treatment approach. Graphical summary of lysophosphatidic signaling in multiple sclerosis.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 45 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 45 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 7 16%
Researcher 7 16%
Student > Ph. D. Student 7 16%
Student > Doctoral Student 4 9%
Student > Bachelor 3 7%
Other 10 22%
Unknown 7 16%
Readers by discipline Count As %
Neuroscience 10 22%
Medicine and Dentistry 8 18%
Biochemistry, Genetics and Molecular Biology 4 9%
Pharmacology, Toxicology and Pharmaceutical Science 4 9%
Chemistry 3 7%
Other 9 20%
Unknown 7 16%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 19 June 2017.
All research outputs
#11,952,539
of 13,481,034 outputs
Outputs from Acta Neuropathologica Communications
#649
of 699 outputs
Outputs of similar age
#226,924
of 268,128 outputs
Outputs of similar age from Acta Neuropathologica Communications
#1
of 1 outputs
Altmetric has tracked 13,481,034 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 699 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.9. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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