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The chicken or the egg? Does glycaemic control predict cognitive function or the other way around?

  • Ithamar Ganmore
  • Michal Schnaider Beeri
Commentary

Abstract

The association between type 2 diabetes and cognitive dysfunction is well established. Prevention of the development of type 2 diabetes and its complications, as well as cognitive dysfunction and dementia, are leading goals in these fields. Deciphering the causality direction of the interplay between type 2 diabetes and cognitive dysfunction, and understanding the timeline of disease progression, are crucial for developing efficient prevention strategies. The prevailing perception is that type 2 diabetes leads to cognitive dysfunction and dementia. There is substantial evidence showing that accelerated cognitive decline in type 2 diabetes starts in midlife (mean age 40–60 years) and that it may even begin at the prediabetes stage. However, in this issue of Diabetologia, Altschul et al (doi:  https://doi.org/10.1007/s00125-018-4645-8) show evidence for the reverse causality hypothesis, i.e. that lower cognitive function precedes poor glycaemic control. They found that cognitive function at early adolescence (age 11 years) predicts both HbA1c levels and cognitive function at age 70 years. Moreover, they found that lower cognitive function at age 70 is associated with an increase in HbA1c from age 70 to 79 years. Based on these findings, future studies should explore whether developing prevention strategies that target young adolescents with lower cognitive function will result in prevention of type 2 diabetes, breaking the vicious cycle of type 2 diabetes and cognitive dysfunction.

Keywords

Adolescence Cognitive decline Cognitive function Dementia Diabetes HbA1c Prevention Type 2 diabetes 

Abbreviations

LBC1936

Lothian Birth Cohort of 1936

MCI

Mild cognitive impairment

Notes

Contribution statement

Both authors were responsible for drafting the article and revising it critically for important intellectual content. Both authors approved the version to be published.

Duality of interest

The authors declare that there is no duality of interest associated with this manuscript.

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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Authors and Affiliations

  1. 1.The Joseph Sagol Neuroscience Center, Sheba Medical CenterRamat GanIsrael
  2. 2.Department of NeurologySheba Medical CenterRamat GanIsrael
  3. 3.Sackler School of MedicineTel-Aviv UniversityTel-AvivIsrael
  4. 4.Department of PsychiatryIcahn School of Medicine at Mount SinaiNew YorkUSA

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