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EMBO reports 5, 5, 527–531 (2004)
doi:10.1038/sj.embor.7400125
Published online: 8 April 2004
Rapid disease development in scrapie-infected mice deficient for CD40 ligand
Michael Burwinkel1, Anja Schwarz1, Constanze Riemer1, Julia Schultz1, Frank van Landeghem2 & Michael Baier1
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1 Project 'Neurodegenerative Diseases', Robert-Koch-Institute, Nordufer 20, 13353 Berlin, Germany
2 Institute of Neuropathology, Humboldt-University, Augustenburger Platz 1, 13353 Berlin, Germany
To whom correspondence should be addressed
Anja Schwarz Tel: +49 30 45472524; Fax: +49 30 45472609; E-mail: schwarza@rki.de
Received 11 July 2003; Accepted 17 February 2004; Published online 8 April 2004.
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Abstract
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- 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.
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