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Unified theory of TSE neurodegeneration

From our observation and published work we believe that:

- PrP binds copper which is essential for its physiological function, but the protein does not deliver per se copper to the cells.
- PrP expression is linked to defence against oxidative stress.
- PrP is involved in signal transduction pathways.
- Dpl, cytosolic and ctm-PrP are not directly involved in TSE neurodegeneration.
- TSE infection results in abnormal copper binding by PrP and susceptibility to oxidative stress.

From these data our unified theory is that PrPSc present during the infection will modified PrP function having for consequences reduced and/or abnormal responses to oxidative stress leading to neurodegeneration.

Reported by

CENTRE NATIONAL DE RECHERCHE SCIENTIFIQUE, UPR 1142
141, rue de la Cardonille
34396 Montpellier
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