Transmissible spongiform encephalopathies (TSEs) are initiated by a novel k
ind of agent that produces characteristic degenerative changes in the brain
without a detectable systemic inflammatory response or serological changes
. A murine scrapie model was evaluated for changes in plasma concentration
of serum amyloid P component (SAP), a protein that is up-regulated in infec
ted and/or injured mice during the acute phase response (APR). C57BL10 and
IRW mice inoculated with scrapie brain developed clinical scrapie 125-150 d
ays later. At this time, concentration of plasma SAP increased in most of t
hem. The SAP level increased greater than or equal to3-fold in >80% of the
scrapie-affected C57BL10 mice and IRW male mice. A similar increase was fou
nd in <3% of respective nonscrapie control mice. The up-regulation of mouse
SAP during clinical scrapie provides evidence for the activation of a syst
emic APR in TSE, a serological change that may be clinically useful.