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Prion protein — mediator of toxicity in multiple proteinopathies

A new study shows that interactions of the cellular prion protein with amyloid-β, tau and α-synuclein oligomers are important in mediating the toxicity of these proteins in Alzheimer disease and Parkinson disease. The findings suggest a shared pathway that could be a therapeutic target common to multiple neurodegenerative diseases.

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  1. Prusiner, S. B. A unifying role for prions in neurodegenerative diseases. Science 336, 1511–1513 (2012).

    Article  CAS  Google Scholar 

  2. Haass, C. & Selkoe, D. J. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer’s amyloid beta-peptide. Nat. Rev. Mol. Cell. Biol. 8, 101–112 (2007).

    Article  CAS  Google Scholar 

  3. Corbett, G. T. et al. PrP is a central player in toxicity mediated by soluble aggregates of neurodegeneration-causing proteins. Acta Neuropathol. 139, 503–526 (2019).

    Article  Google Scholar 

  4. Bessen, R. A. & Marsh, R. F. Distinct PrP properties suggest the molecular basis of strain variation in transmissible mink encephalopathy. J. Virol. 68, 7859–7868 (1994).

    Article  CAS  Google Scholar 

  5. Smith, L. M., Kostylev, M. A., Lee, S. & Strittmatter, S. M. Systematic and standardized comparison of reported amyloid-beta receptors for sufficiency, affinity, and Alzheimer’s disease relevance. J. Biol. Chem. 294, 6042–6053 (2019).

    Article  CAS  Google Scholar 

  6. Guerrero-Ferreira, R. et al. Two new polymorphic structures of human full-length alpha-synuclein fibrils solved by cryo-electron microscopy. eLife 8, e48907 (2019).

    Article  Google Scholar 

  7. Zhang, W. et al. Heparin-induced tau filaments are polymorphic and differ from those in Alzheimer’s and Pick’s diseases. eLife 8, e43584 (2019).

    Article  Google Scholar 

  8. Um, J. W. et al. Metabotropic glutamate receptor 5 is a coreceptor for Alzheimer Aβ oligomer bound to cellular prion protein. Neuron 79, 887–902 (2013).

    Article  CAS  Google Scholar 

  9. Friberg, K. N. et al. Intracerebral infusion of antisense oligonucleotides into prion-infected mice. Mol. Ther. Nucleic Acids 1, e9 (2012).

    Article  Google Scholar 

  10. Raymond, G. J. et al. Antisense oligonucleotides extend survival of prion-infected mice. JCI Insight 5, 131175 (2019).

    Article  Google Scholar 

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The authors thank Nick A. Paras for useful discussions.

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Correspondence to Stanley B. Prusiner.

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The Institute for Neurodegenerative Diseases has a research collaboration with Daiichi Sankyo (Tokyo, Japan). S.B.P. is a member of the Scientific Advisory Board of ViewPoint Therapeutics and a member of the Board of Directors of Trizell. J.I.A. declares no competing interests.

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Ayers, J.I., Prusiner, S.B. Prion protein — mediator of toxicity in multiple proteinopathies. Nat Rev Neurol 16, 187–188 (2020).

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