Figures & data
Figure 1. Prion-like mechanisms in Alzheimer disease. Amyloid-β (Aβ) peptides can form toxic oligomers that are able to propogate by a prion-like mechanism of template-mediated protein misfolding. Aβ oligomers can activate tau kinases, which then catalyze pathogenic phosphorylation of tau (pTau), and may also serve as prion-like seeds that induce tau to oligomerize. Tau oligomers also self-propogate by a prion-like mechanism, and along with pathogenically phosphorylated tau, drive the degeneration and death of neurons involved in memory and cognition. The temporal and functional relationships between pathogenic phosphorylation and oligomerization of tau remain to be determined.
![Figure 1. Prion-like mechanisms in Alzheimer disease. Amyloid-β (Aβ) peptides can form toxic oligomers that are able to propogate by a prion-like mechanism of template-mediated protein misfolding. Aβ oligomers can activate tau kinases, which then catalyze pathogenic phosphorylation of tau (pTau), and may also serve as prion-like seeds that induce tau to oligomerize. Tau oligomers also self-propogate by a prion-like mechanism, and along with pathogenically phosphorylated tau, drive the degeneration and death of neurons involved in memory and cognition. The temporal and functional relationships between pathogenic phosphorylation and oligomerization of tau remain to be determined.](/cms/asset/9bbb8a60-c126-4cac-a660-d0016aabf840/kprn_a_10922118_f0001.gif)