Abstract
Is it all about Contact? Neurodegeneration as a “Protein Freeze Tag Game” Inside the Central Nervous System
Highlights
The so-called “prion hypothesis” for explaining spongiform encephalopathies is classically attributed to Prusiner, who in 1982 suggested that the scrapie agent was a proteinaceous infectious particle which would be resistant to known methods of nucleic acids inactivation (Prusiner, 1982)
As protein polymerization with subsequent formation of deposit aggregates have been implied in the pathogenesis of several degenerative processes in the central nervous system (CNS), it was logical to suppose that the underlying pathogenesis of these diseases might have some similarity with the aforementioned “polymer
As several similarities exist between induction of β-amyloid deposits was inithe pathophysiology of systemic and CNS tially most evident within the injected area, amyloidoses, there has been a growing inter- recent cross-sectional autopsy studies have est in the experimental evaluation of a pos- demonstrated that the accumulation of sible protein-to-protein contact-induced misfolded proteins follows a characteristic transmission as the pathophysiological and predictable pattern of spatial progresexplanation for the progression of neuro- sion in the brain of patients affected by AD
Summary
The so-called “prion hypothesis” for explaining spongiform encephalopathies is classically attributed to Prusiner, who in 1982 suggested that the scrapie agent was a proteinaceous infectious particle which would be resistant to known methods of nucleic acids inactivation (Prusiner, 1982). Kanouchi et al, 2012) have suggested that promoted the aggregation and deposition the basic proteins implied in a variety of of β-amyloid in the injected brain (Kane neurodegenerative diseases [like beta- et al, 2000).
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