Mechanisms of prion diseases described as long-lasting disorders of the blood-brain barrier system.
Prison diseases can be described as disorders wherein circulating prion molecules of external origin intervene with the normal synthesis of similar molecules in the central nervous system. The hypothesis is that the endogenous prion-like molecules denote the blood-brain barrier discontinuity. In the case of barrier discontinuity, small numbers of hypothetical signal molecules enter circulation and attach to the receptor sites in the neighbouring blood vessels. The specific receptors of the cells in the blood vessels stimulated by endogenous prion-like molecules might initiate the repairing processes of the blood-brain barrier. In prion diseases, prion molecules from external sources are similar to endogenous prion-like molecules or to the hypothetical signal molecules described here. Large numbers of prion molecules enter circulation and initiate repairing processes in large brain areas causing the tissue damage. This damage leads to new barrier discontinuities that would provoke pathological process even when the exogenous prion molecules are no longer present in the circulation.
Kurbel
S
S
Department of Oncology, Osijek Clinical Hospital, Croatia.
Kurbel
B
B
D000818:Animals; D001812:Blood-Brain Barrier / Q000502:physiology*; D001921:Brain / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D017096:Prion Diseases / Q000209:etiology* / Q000503:physiopathology; D011328:Prions / Q000378:metabolism; D015398:Signal Transduction
D011328:Prions