Abstract
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy.
Highlights
With incubation time ranging from 5 to 40 years, Creutzfeldt-Jakob disease (CJD) is a deadly condition caused by the accumulation of toxic forms of the prion protein in the brain
Multiple studies were published linking amyloid-β (Aβ) deposits in the brain—a key feature of Alzheimer’s disease (AD)—to prion disease patients that acquired it through several different sources (Watanabe and Duchen, 1993; Preusser et al, 2006; Tousseyn et al, 2015)
Both Aβ deposits and prion protein deposits occurs by a nucleation-dependent polymerization process in which oligomeric “seed” proteins trigger the formation of an ordered nucleus that may rapidly grows into larger polymer fibrils (Harper and Lansbury, 1997)
Summary
With incubation time ranging from 5 to 40 years, Creutzfeldt-Jakob disease (CJD) is a deadly condition caused by the accumulation of toxic forms of the prion protein in the brain. A commentary on Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy by Jaunmuktane, Z., Mead, S., Ellis, M., Wadsworth, J. Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy.
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