Plasma noradrenalin as marker of neuroinvasion in prion diseases

In order to study the effects of PrP neuroinvasion on sympathetic nerve function, plasma catecholamine levels in intraperitoneal (i.p.) and intracerebral (i.c.) infected hamsters have been determined. The results of this study clearly indicate a specific altered sympathetic nerve function because the levels of noradrenaline (but not adrenaline) were markedly increased in the animals infected peripherally, but not in those infected intracerebrally. This finding confirms the fact that, in a subsequent phase, prion neuroinvasion uses the SNS to spread from the periphery to the CNS after invading LRS organs, such as the spleen. Although the mechanism of peripheral nerve prion transport is not fully understood, the present results indicate that prions markedly perturb the nerve terminals, thus leading to an increase in noradrenaline turnover.