Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1 - 11 |
| Number of pages | 11 |
| Journal | Journal of Neuroinflammation |
| Volume | 11 |
| Issue number | (Art. No: 37) |
| DOIs | |
| Publication status | Published - 2014 |
Cite this
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Anti-lysophosphatidic acid antibodies improve traumatic brain injury outcomes. / Crack, Peter J; Zhang, Moses; Morganti-Kossmann, Maria Cristina; Morris, Andrew; Wojciak, Jonathan M; Fleming, Jonathan K; Karve, Ila; Wright, David K; Sashindranath, Maithili; Goldshmit, Yona; Conquest, Alison; Daglas, Maria; Johnston, Leigh Andrea; Medcalf, Robert Lindsay; Sabbadini, Roger A; Pebay, Alice.
In: Journal of Neuroinflammation, Vol. 11, No. (Art. No: 37), 2014, p. 1 - 11.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Anti-lysophosphatidic acid antibodies improve traumatic brain injury outcomes
AU - Crack, Peter J
AU - Zhang, Moses
AU - Morganti-Kossmann, Maria Cristina
AU - Morris, Andrew
AU - Wojciak, Jonathan M
AU - Fleming, Jonathan K
AU - Karve, Ila
AU - Wright, David K
AU - Sashindranath, Maithili
AU - Goldshmit, Yona
AU - Conquest, Alison
AU - Daglas, Maria
AU - Johnston, Leigh Andrea
AU - Medcalf, Robert Lindsay
AU - Sabbadini, Roger A
AU - Pebay, Alice
PY - 2014
Y1 - 2014
N2 - Background: Lysophosphatidic acid (LPA) is a bioactive phospholipid with a potentially causative role in neurotrauma. Blocking LPA signaling with the LPA-directed monoclonal antibody B3/Lpathomab is neuroprotective in the mouse spinal cord following injury. FINDINGS: Here we investigated the use of this agent in treatment of secondary brain damage consequent to traumatic brain injury (TBI). LPA was elevated in cerebrospinal fluid (CSF) of patients with TBI compared to controls. LPA levels were also elevated in a mouse controlled cortical impact (CCI) model of TBI and B3 significantly reduced lesion volume by both histological and MRI assessments. Diminished tissue damage coincided with lower brain IL-6 levels and improvement in functional outcomes. Conclusions: This study presents a novel therapeutic approach for the treatment of TBI by blocking extracellular LPA signaling to minimize secondary brain damage and neurological dysfunction.
AB - Background: Lysophosphatidic acid (LPA) is a bioactive phospholipid with a potentially causative role in neurotrauma. Blocking LPA signaling with the LPA-directed monoclonal antibody B3/Lpathomab is neuroprotective in the mouse spinal cord following injury. FINDINGS: Here we investigated the use of this agent in treatment of secondary brain damage consequent to traumatic brain injury (TBI). LPA was elevated in cerebrospinal fluid (CSF) of patients with TBI compared to controls. LPA levels were also elevated in a mouse controlled cortical impact (CCI) model of TBI and B3 significantly reduced lesion volume by both histological and MRI assessments. Diminished tissue damage coincided with lower brain IL-6 levels and improvement in functional outcomes. Conclusions: This study presents a novel therapeutic approach for the treatment of TBI by blocking extracellular LPA signaling to minimize secondary brain damage and neurological dysfunction.
UR - http://www.jneuroinflammation.com/content/pdf/1742-2094-11-37.pdf
U2 - 10.1186/1742-2094-11-37
DO - 10.1186/1742-2094-11-37
M3 - Article
VL - 11
SP - 1
EP - 11
JO - Journal of Neuroinflammation
JF - Journal of Neuroinflammation
SN - 1742-2094
IS - (Art. No: 37)
ER -