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Review
. 2020 Apr 15;21(8):2744.
doi: 10.3390/ijms21082744.

The Interplay between Diabetes and Alzheimer's Disease-In the Hunt for Biomarkers

Affiliations
Review

The Interplay between Diabetes and Alzheimer's Disease-In the Hunt for Biomarkers

Adriana Kubis-Kubiak et al. Int J Mol Sci. .

Abstract

The brain is an organ in which energy metabolism occurs most intensively and glucose is an essential and dominant energy substrate. There have been many studies in recent years suggesting a close relationship between type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) as they have many pathophysiological features in common. The condition of hyperglycemia exposes brain cells to the detrimental effects of glucose, increasing protein glycation and is the cause of different non-psychiatric complications. Numerous observational studies show that not only hyperglycemia but also blood glucose levels near lower fasting limits (72 to 99 mg/dL) increase the incidence of AD, regardless of whether T2DM will develop in the future. As the comorbidity of these diseases and earlier development of AD in T2DM sufferers exist, new AD biomarkers are being sought for etiopathogenetic changes associated with early neurodegenerative processes as a result of carbohydrate disorders. The S100B protein seem to be interesting in this respect as it may be a potential candidate, especially important in early diagnostics of these diseases, given that it plays a role in both carbohydrate metabolism disorders and neurodegenerative processes. It is therefore necessary to clarify the relationship between the concentration of the S100B protein and glucose and insulin levels. This paper draws attention to a valuable research objective that may in the future contribute to a better diagnosis of early neurodegenerative changes, in particular in subjects with T2DM and may be a good basis for planning experiments related to this issue as well as a more detailed explanation of the relationship between the neuropathological disturbances and changes of glucose and insulin concentrations in the brain.

Keywords: Alzheimer’s disease; S100 proteins; biomarkers; diabetes mellitus.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Consequences of acute hyperglycemia action in the brain.
Figure 2
Figure 2
The effect of S100B high concentrations on neurodegeneration processes.

References

    1. Chatterjee S., Mudher A. Alzheimer’s disease and type 2 diabetes: A critical assessment of the shared pathological traits. Front. Neurosci. 2018 doi: 10.3389/fnins.2018.00383. - DOI - PMC - PubMed
    1. Haass C. Take five—BACE and the γ-secretase quartet conduct Alzheimer’s amyloid β-peptide generation. EMBO J. 2004 doi: 10.1038/sj.emboj.7600061. - DOI - PMC - PubMed
    1. Alonso A.D., Cohen L.S., Corbo C., Morozova V., ElIdrissi A., Phillips G., Kleiman F.E. Hyperphosphorylation of Tau Associates With Changes in Its Function Beyond Microtubule Stability. Front. Cell. Neurosci. 2018;12:1–11. doi: 10.3389/fncel.2018.00338. - DOI - PMC - PubMed
    1. Laßek M., Weingarten J., Einsfelder U., Brendel P., Müller U., Volknandt W. Amyloid precursor proteins are constituents of the presynaptic active zone. J. Neurochem. 2013 doi: 10.1111/jnc.12358. - DOI - PubMed
    1. Wang Z., Wang B., Yang L., Guo Q., Aithmitti N., Songyang Z., Zheng H. Presynaptic and Postsynaptic Interaction of the Amyloid Precursor Protein Promotes Peripheral and Central Synaptogenesis. J. Neurosci. 2009 doi: 10.1523/JNEUROSCI.2132-09.2009. - DOI - PMC - PubMed

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