Details

Autor(en) / Beteiligte

• LaCasse, Rachel A
• Striebel, James F
• Favara, Cynthia
• Kercher, Lisa
• Chesebro, Bruce

Titel

Role of Erk1/2 activation in prion disease pathogenesis: Absence of CCR1 leads to increased Erk1/2 activation and accelerated disease progression

Ist Teil von

• Journal of neuroimmunology, 2008-05, Vol.196 (1), p.16-26

Ort / Verlag

Netherlands: Elsevier B.V

Erscheinungsjahr

2008

Quelle

Elsevier ScienceDirect Journals

Beschreibungen/Notizen

• Abstract 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.