Evidence for this hypothesis:

Infectivity titre correlates with PrPSc levels. However, this is disputed. PrPSc is an isomer of PrPC
Denaturing PrP removes infectivity
PrP-null mice cannot be infected
PrPC depletion in the neural system of mice with established neuroinvasive prion infection reverses early spongeosis and behavioural deficits, halts further disease progression and increases life-span

Multi-component hypothesis
While not containing a nucleic acid genome, prions may be composed of more than just a protein. Purified PrPC appears unable to convert to the infectious PrPSc form, unless other components are added, such as RNA and lipids. These other components, termed cofactors, may form part of the infectious prion, or they may serve as catalysts for the replication of a protein-only prion. Viral hypothesis
This hypothesis postulates that an as of yet undiscovered infectious viral agent is the cause of the disease. Evidence for this hypothesis is as follows:

Incubation time is comparable to a lentivirus
Strain variation of different isolates of PrPSc
An increasing titre of PrPSc as the disease progresses suggests a replicating agent. Diagnosis
There continues to be a very practical problem with diagnosis of prion diseases, including BSE and CJD. They have an incubation period of months to decades during which there are no symptoms, even though the pathway of converting the normal brain PrP protein into the toxic, disease-related PrPSc form has started. At present, there is virtually no way to detect PrPSc reliably except by examining the brain using neuropathological and immunohistochemical methods after death.
Dysfunction can refer to:

Abnormality (behavior)
Dysfunctional family
Sexual dysfunction
Dysfunction (album), an album by the rock band Staind
Manifest and latent functions and dysfunctions (sociological theory)
Measurement dysfunction

See also
Malfunction (disambiguation)