| First Author | Joy MT | Year | 2019 |
| Journal | Cell | Volume | 176 |
| Issue | 5 | Pages | 1143-1157.e13 |
| PubMed ID | 30794775 | Mgi Jnum | J:271340 |
| Mgi Id | MGI:6281079 | Doi | 10.1016/j.cell.2019.01.044 |
| Citation | Joy MT, et al. (2019) CCR5 Is a Therapeutic Target for Recovery after Stroke and Traumatic Brain Injury. Cell 176(5):1143-1157.e13 |
| abstractText | We tested a newly described molecular memory system, CCR5 signaling, for its role in recovery after stroke and traumatic brain injury (TBI). CCR5 is uniquely expressed in cortical neurons after stroke. Post-stroke neuronal knockdown of CCR5 in pre-motor cortex leads to early recovery of motor control. Recovery is associated with preservation of dendritic spines, new patterns of cortical projections to contralateral pre-motor cortex, and upregulation of CREB and DLK signaling. Administration of a clinically utilized FDA-approved CCR5 antagonist, devised for HIV treatment, produces similar effects on motor recovery post stroke and cognitive decline post TBI. Finally, in a large clinical cohort of stroke patients, carriers for a naturally occurring loss-of-function mutation in CCR5 (CCR5-Delta32) exhibited greater recovery of neurological impairments and cognitive function. In summary, CCR5 is a translational target for neural repair in stroke and TBI and the first reported gene associated with enhanced recovery in human stroke. |
