Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Brief Communication
  • Published:

Amyloid-β transmission or unexamined bias?

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Causal diagram depicting the proposed causal pathways, the authors’ interpretation, the two confounding biases and the inconclusive conditioning on presence of prion disease.

References

  1. Jaunmuktane, Z. et al. Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy. Nature 525, 247–250 (2015)

    Article  CAS  ADS  Google Scholar 

  2. Nyberg, F. & Hallberg, M. Growth hormone and cognitive function. Nat. Rev. Endocrinol. 9, 357–365 (2013)

    Article  CAS  Google Scholar 

  3. Gasparini, L. & Xu, H. Potential roles of insulin and IGF-1 in Alzheimer’s disease. Trends Neurosci. 26, 404–406 (2003)

    Article  CAS  Google Scholar 

  4. Westwood, A. J. et al. Insulin-like growth factor-1 and risk of Alzheimer dementia and brain atrophy. Neurology 82, 1613–1619 (2014)

    Article  CAS  Google Scholar 

  5. Carro, E., Trejo, J. L., Gomez-Isla, T., LeRoith, D. & Torres-Aleman, I. Serum insulin-like growth factor I regulates brain amyloid-β levels. Nat. Med. 8, 1390–1397 (2002)

    Article  CAS  Google Scholar 

  6. Araki, W., Kume, H., Oda, A., Tamaoka, A. & Kametani, F. IGF-1 promotes β-amyloid production by a secretase-independent mechanism. Biochem. Biophys. Res. Commun. 380, 111–114 (2009)

    Article  CAS  Google Scholar 

  7. Trejo, J. L., Carro, E., Garcia-Galloway, E. & Torres-Aleman, I. Role of insulin-like growth factor I signaling in neurodegenerative diseases. J. Mol. Med. (Berl.) 82, 156–162 (2004)

    Article  CAS  Google Scholar 

  8. Mustafa, A. et al. Decreased plasma insulin-like growth factor-I level in familial Alzheimer’s disease patients carrying the Swedish APP 670/671 mutation. Dement. Geriatr. Cogn. Disord. 10, 446–451 (1999)

    Article  CAS  Google Scholar 

  9. Tham, A. et al. Insulin-like growth factors and insulin-like growth factor binding proteins in cerebrospinal fluid and serum of patients with dementia of the Alzheimer type. J. Neural Transm. Park. Dis. Dement. Sect. 5, 165–176 (1993)

    Article  CAS  Google Scholar 

  10. Hainfellner, J. A. et al. Coexistence of Alzheimer-type neuropathology in Creutzfeldt–Jakob disease. Acta Neuropathol. 96, 116–122 (1998)

    Article  CAS  Google Scholar 

  11. Greenland, S., Pearl, J. & Robins, J. M. Causal diagrams for epidemiologic research. Epidemiology 10, 37–48 (1999)

    Article  CAS  Google Scholar 

  12. Abbott, A. The red-hot debate about transmissible Alzheimer’s. Nature 531, 294–297 (2016)

    Article  CAS  ADS  Google Scholar 

  13. Rothman, K. J., Greenland, S. & Lash, T. L. Modern epidemiology (Lippincott Williams & Wilkins, 2008)

  14. Hernán, M. A. & Robins, J. M. Causal Inference (Boca Raton: Chapman & Hall/CRC) (https://www.hsph.harvard.edu/miguel-hernan/causal-inference-book/) (in the press)

Download references

Author information

Authors and Affiliations

Authors

Contributions

All authors contributed to the study and to the writing of this Brief Communication Arising.

Corresponding author

Correspondence to M. Arfan Ikram.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

PowerPoint slides

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

H. Adams, H., A. Swanson, S., Hofman, A. et al. Amyloid-β transmission or unexamined bias?. Nature 537, E7–E9 (2016). https://doi.org/10.1038/nature19086

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nature19086

This article is cited by

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing