Top

Published in:

01-06-2018 | Correspondence

Infectious prions do not induce Aβ deposition in an in vivo seeding model

Authors: Jay Rasmussen, Susanne Krasemann, Hermann Altmeppen, Petra Schwarz, Juliane Schelle, Adriano Aguzzi, Markus Glatzel, Mathias Jucker

Published in: Acta Neuropathologica | Issue 6/2018

Excerpt

An increasing number of studies have suggested that certain cases of iatrogenic Creutzfeldt–Jakob disease (iCJD) that harbor significant β-amyloid (Aβ) pathology are the result of aggregated Aβ transmission to patients during the same procedure that caused prion disease [2, 4, 7, 8, 11, 13, 17]. The source of iatrogenic contamination has been observed both for human growth hormone infusions and dura mater grafts, arguing against a treatment specific effect. Intriguingly, recent work has also observed suspected Aβ pathology transmission in post-mortem samples that received growth hormone treatments but did not develop CJD [17]. Yet another study suggested that neurosurgery with Aβ-contaminated tools can transmit Aβ pathology and lead to intracerebral hemorrhage [12]. These findings have been debated in the context of whether Aβ pathology is truly transmissible and whether Alzheimer’s disease could subsequently develop. …

Available only for authorised users

Bueler H, Fischer M, Lang Y, Bluethmann H, Lipp HP, DeArmond SJ, Prusiner SB, Aguet M, Weissmann C (1992) Normal development and behaviour of mice lacking the neuronal cell-surface PrP protein. Nature 356:577–582. https://doi.org/10.1038/356577a0 CrossRefPubMed

Cali I, Cohen ML, Hasmall Yi US, Parchi P, Giaccone G, Collins SJ, Kofskey D, Wang H, McLean CA, Brandel JP et al (2018) Iatrogenic Creutzfeldt-Jakob disease with Amyloid-beta pathology: an international study. Acta Neuropathol Commun 6:5. https://doi.org/10.1186/s40478-017-0503-z CrossRefPubMedPubMedCentral

Dohler F, Sepulveda-Falla D, Krasemann S, Altmeppen H, Schluter H, Hildebrand D, Zerr I, Matschke J, Glatzel M (2014) High molecular mass assemblies of amyloid-beta oligomers bind prion protein in patients with Alzheimer’s disease. Brain 137:873–886. https://doi.org/10.1093/brain/awt375 CrossRefPubMed

Duyckaerts C, Sazdovitch V, Ando K, Seilhean D, Privat N, Yilmaz Z, Peckeu L, Amar E, Comoy E, Maceski A et al (2018) Neuropathology of iatrogenic Creutzfeldt-Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology. Acta Neuropathol 135:201–212. https://doi.org/10.1007/s00401-017-1791-x CrossRefPubMed

Eisele YS, Obermuller U, Heilbronner G, Baumann F, Kaeser SA, Wolburg H, Walker LC, Staufenbiel M, Heikenwalder M, Jucker M (2010) Peripherally applied Abeta-containing inoculates induce cerebral beta-amyloidosis. Science 330:980–982. https://doi.org/10.1126/science.1194516 CrossRefPubMedPubMedCentral

Fischer M, Rulicke T, Raeber A, Sailer A, Moser M, Oesch B, Brandner S, Aguzzi A, Weissmann C (1996) Prion protein (PrP) with amino-proximal deletions restoring susceptibility of PrP knockout mice to scrapie. EMBO J 15:1255–1264PubMedPubMedCentralCrossRef

Frontzek K, Lutz MI, Aguzzi A, Kovacs GG, Budka H (2016) Amyloid-beta pathology and cerebral amyloid angiopathy are frequent in iatrogenic Creutzfeldt-Jakob disease after dural grafting. Swiss Med Wkly 146:w14287. https://doi.org/10.4414/smw.2016.14287 PubMedCrossRef

Hamaguchi T, Taniguchi Y, Sakai K, Kitamoto T, Takao M, Murayama S, Iwasaki Y, Yoshida M, Shimizu H, Kakita A et al (2016) Significant association of cadaveric dura mater grafting with subpial Abeta deposition and meningeal amyloid angiopathy. Acta Neuropathol 132:313–315. https://doi.org/10.1007/s00401-016-1588-3 CrossRefPubMed

Hainfellner JA, Wanschitz J, Jellinger K, Liberski PP, Gullotta F, Budka H (1998) Coexistence of Alzheimer-type neuropathology in Creutzfeldt-Jakob disease. Acta Neuropathol 96:116–122CrossRefPubMed

10.

Herve D, Porche M, Cabrejo L, Guidoux C, Tournier-Lasserve E, Nicolas G, Adle-Biassette H, Plu I, Chabriat H, Duyckaerts C (2018) Fatal Abeta cerebral amyloid angiopathy 4 decades after a dural graft at the age of 2 years. Acta Neuropathol. https://doi.org/10.1007/s00401-018-1828-9 PubMedCrossRef

11.

Jaunmuktane Z, Mead S, Ellis M, Wadsworth JD, Nicoll AJ, Kenny J, Launchbury F, Linehan J, Richard-Loendt A, Walker AS et al (2015) Evidence for human transmission of amyloid-beta pathology and cerebral amyloid angiopathy. Nature 525:247–250. https://doi.org/10.1038/nature15369 CrossRefPubMed

12.

Jaunmuktane Z, Quaegebeur A, Taipa R, Viana-Baptista M, Barbosa R, Koriath C, Sciot R, Mead S, Brandner S (2018) Evidence of amyloid-beta cerebral amyloid angiopathy transmission through neurosurgery. Acta Neuropathol. https://doi.org/10.1007/s00401-018-1822-2 PubMedCentralCrossRefPubMed

13.

Kovacs GG, Lutz MI, Ricken G, Strobel T, Hoftberger R, Preusser M, Regelsberger G, Honigschnabl S, Reiner A, Fischer P et al (2016) Dura mater is a potential source of Abeta seeds. Acta Neuropathol 131:911–923. https://doi.org/10.1007/s00401-016-1565-x CrossRefPubMedPubMedCentral

14.

Lauren J, Gimbel DA, Nygaard HB, Gilbert JW, Strittmatter SM (2009) Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers. Nature 457:1128–1132. https://doi.org/10.1038/nature07761 CrossRefPubMedPubMedCentral

15.

Meyer-Luehmann M, Coomaraswamy J, Bolmont T, Kaeser S, Schaefer C, Kilger E, Neuenschwander A, Abramowski D, Frey P, Jaton AL et al (2006) Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host. Science 313:1781–1784. https://doi.org/10.1126/science.1131864 CrossRefPubMed

16.

Morales R, Estrada LD, Diaz-Espinoza R, Morales-Scheihing D, Jara MC, Castilla J, Soto C (2010) Molecular cross talk between misfolded proteins in animal models of Alzheimer’s and prion diseases. J Neurosci 30:4528–4535. https://doi.org/10.1523/JNEUROSCI.5924-09.2010 CrossRefPubMedPubMedCentral

17.

Ritchie DL, Adlard P, Peden AH, Lowrie S, Le Grice M, Burns K, Jackson RJ, Yull H, Keogh MJ, Wei W et al (2017) Amyloid-beta accumulation in the CNS in human growth hormone recipients in the UK. Acta Neuropathol 134:221–240. https://doi.org/10.1007/s00401-017-1703-0 CrossRefPubMedPubMedCentral

18.

Sarell CJ, Quarterman E, Yip DC, Terry C, Nicoll AJ, Wadsworth JDF, Farrow MA, Walsh DM, Collinge J (2017) Soluble Abeta aggregates can inhibit prion propagation. Open Biol. https://doi.org/10.1098/rsob.170158 PubMedPubMedCentralCrossRef

19.

Schwarze-Eickner K, Keyvani K, Görtz N, Westaway D, Sachser D, Paulus W (2005) Prion protein (PrPc) promotes beta-amyloid plaque formation. Neurobiol Aging 26:1177–1182CrossRef

20.

Ye L, Rasmussen J, Kaeser SA, Marzesco AM, Obermuller U, Mahler J, Schelle J, Odenthal J, Kruger C, Fritschi SK et al (2017) Abeta seeding potency peaks in the early stages of cerebral beta-amyloidosis. EMBO Rep 18:1536–1544. https://doi.org/10.15252/embr.201744067 CrossRefPubMedPubMedCentral

Title: Infectious prions do not induce Aβ deposition in an in vivo seeding model
Authors: Jay Rasmussen
Susanne Krasemann
Hermann Altmeppen
Petra Schwarz
Juliane Schelle
Adriano Aguzzi
Markus Glatzel
Mathias Jucker
Publication date: 01-06-2018
Publisher: Springer Berlin Heidelberg
Published in: Acta Neuropathologica / Issue 6/2018
Print ISSN: 0001-6322
Electronic ISSN: 1432-0533
DOI: https://doi.org/10.1007/s00401-018-1848-5

At a glance: The ONWARDS insulin icodec trials

Springer Medicine

Infectious prions do not induce Aβ deposition in an in vivo seeding model

Excerpt

At a glance: The ONWARDS insulin icodec trials

Springer Medicine

Excerpt

Please log in to get access to this content

Other articles of this Issue 6/2018

The relationship between neurosurgical instruments and disease transmission: Society of British Neurological Surgeons perspective

An intronic VNTR affects splicing of ABCA7 and increases risk of Alzheimer’s disease

Mutations in LRRK2 amplify cell-to-cell protein aggregate propagation: a hypothesis

Interaction of amyloidogenic proteins in pancreatic β cells from subjects with synucleinopathies

Evidence for altered dendritic spine compartmentalization in Alzheimer’s disease and functional effects in a mouse model

Genomic analysis reveals secondary glioblastoma after radiotherapy in a subset of recurrent medulloblastomas