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ALZHEIMER DISEASE

Amyloid-β — a reflection of risk or a preclinical marker?

Nature Reviews Neurology volume 14, pages 319–320 (2018)Cite this article

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In a recent study, individuals with brain amyloid-β accumulation but no cognitive impairment were classified as being at risk of Alzheimer disease, yet amyloid-β is widely considered to be a pathological biomarker of Alzheimer disease rather than a risk factor — it cannot be both.

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References

  1. Dubois, B. et al. Cognitive and neuroimaging features and brain beta-amyloidosis in individuals at risk of Alzheimer’s disease (INSIGHT-preAD): a longitudinal observational study. Lancet Neurol. 17, 335–346 (2018).

    Article  PubMed  CAS  Google Scholar 

  2. Sperling, R. A. et al. Toward defining the preclinical stages of Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 7, 280–292 (2011).

    Article  PubMed  PubMed Central  Google Scholar 

  3. Vemuri, P. et al. Cognitive reserve and Alzheimer’s disease biomarkers are independent determinants of cognition. Brain 134, 1479–1492 (2011).

    Article  PubMed  PubMed Central  Google Scholar 

  4. Baker, J. E. et al. Cognitive impairment and decline in cognitively normal older adults with high amyloid-beta: a meta-analysis. Alzheimers Dement. (Amst.) 6, 108–121 (2017).

    Google Scholar 

  5. Donohue, M. C. et al. Association between elevated brain amyloid and subsequent cognitive decline among cognitively normal persons. JAMA 317, 2305–2316 (2017).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  6. Vos, S. J. et al. Preclinical Alzheimer’s disease and its outcome: a longitudinal cohort study. Lancet Neurol. 12, 957–965 (2013).

    Article  PubMed  PubMed Central  Google Scholar 

  7. Montine, T. J. et al. National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach. Acta Neuropathol. 123, 1–11 (2012).

    Article  PubMed  CAS  Google Scholar 

  8. Jack, C. R. Jr. et al. Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade. Lancet Neurol. 9, 119–128 (2010).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  9. Jack, C. R. Jr. et al. Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol. 12, 207–216 (2013).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  10. Kaufman, S. K. et al. Tau prion strains dictate patterns of cell pathology, progression rate, and regional vulnerability in vivo. Neuron 92, 796–812 (2016).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

Download references

Acknowledgements

The authors wish to acknowledge the following for funding support: National Institutes of Health (R01 AG011378, R01 AG041851, R01 NS097495, R01 AG056366) and the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Clinic.

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Authors and Affiliations

  1. Department of Radiology, Mayo Clinic, Rochester, MN, USA

    Clifford R. Jack Jr & Prashanthi Vemuri

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  1. Clifford R. Jack Jr
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  2. Prashanthi Vemuri
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Correspondence to Clifford R. Jack Jr.

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The authors declare no competing interests.

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Jack, C.R., Vemuri, P. Amyloid-β — a reflection of risk or a preclinical marker?. Nat Rev Neurol 14, 319–320 (2018). https://doi.org/10.1038/s41582-018-0008-9

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