| First Author | Burwinkel M | Year | 2004 |
| Journal | EMBO Rep | Volume | 5 |
| Issue | 5 | Pages | 527-31 |
| PubMed ID | 15071493 | Mgi Jnum | J:115487 |
| Mgi Id | MGI:3691766 | Doi | 10.1038/sj.embor.7400125 |
| Citation | Burwinkel M, et al. (2004) Rapid disease development in scrapie-infected mice deficient for CD40 ligand. EMBO Rep 5(5):527-31 |
| abstractText | The inhibition of CD40-CD40L interaction-mediated signalling was suggested as a therapeutic strategy for the treatment of Alzheimer's disease. Conversely, CD40-deficient neurons were reported to be more vulnerable to stress associated with ageing as well as nerve growth factor-beta and serum withdrawal. We studied the scrapie infection of CD40L-deficient (CD40L(-/-)) mice to see whether ablation of the CD40L gene would be beneficial or detrimental in this model of a neurodegenerative amyloidosis. CD40L(-/-) mice died on average 40 days earlier than wild-type control mice and exhibited a more pronounced vacuolation of the neuropil and an increased microglia activation. The experimental model indicates that a deficiency for CD40L is highly detrimental in prion diseases and reinforces the neuroprotective function of intact CD40-CD40L interactions. The stimulation of neuroprotective pathways may represent a possibility to delay therapeutically the disease onset in prion infections of the central nervous system. |
