| First Author | LaCasse RA | Year | 2008 |
| Journal | J Neuroimmunol | Volume | 196 |
| Issue | 1-2 | Pages | 16-26 |
| PubMed ID | 18396336 | Mgi Jnum | J:139922 |
| Mgi Id | MGI:3810608 | Doi | 10.1016/j.jneuroim.2008.02.009 |
| Citation | LaCasse RA, et al. (2008) Role of Erk1/2 activation in prion disease pathogenesis: absence of CCR1 leads to increased Erk1/2 activation and accelerated disease progression. J Neuroimmunol 196(1-2):16-26 |
| abstractText | Prion diseases are neurodegenerative infections with gliosis and vacuolation. The mechanisms of degeneration remain unclear, but chemokines may be important. In current experiments CCR1 knock-out (KO) mice succumbed more rapidly to scrapie infection than WT controls. Infected KO mice had upregulation of CCL3, a CCR1 ligand, and CCR5, a receptor with specificity for CCL3. Both infected KO and WT mice had upregulation of CCR5-mediated signaling involving activation of Erk1/2 in astrocytes; however, activation was earlier in KO mice suggesting a role in pathogenesis. In both mouse strains activation of the Erk1/2 pathway may lead to astrocyte dysfunction resulting in neurodegeneration. |
