Document Type

Journal Article

Publication Title

International Journal of Molecular Sciences

ISSN

16616596

Volume

21

Issue

21

First Page

1

Last Page

20

Publisher

MDPI

School

School of Medical and Health Sciences

Funders

Torrens University Australia Curtin University

Comments

Rowles, J. E., Keane, K. N., Gomes Heck, T., Cruzat, V., Verdile, G., & Newsholme, P. (2020). Are heat shock proteins an important link between type 2 diabetes and Alzheimer disease?. International Journal of Molecular Sciences, 21(21), article 8204. https://doi.org/10.3390/ijms21218204

Abstract

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Type 2 diabetes (T2D) and Alzheimer’s disease (AD) are growing in prevalence worldwide. The development of T2D increases the risk of AD disease, while AD patients can show glucose imbalance due to an increased insulin resistance. T2D and AD share similar pathological features and underlying mechanisms, including the deposition of amyloidogenic peptides in pancreatic islets (i.e., islet amyloid polypeptide; IAPP) and brain (β-Amyloid; Aβ). Both IAPP and Aβ can undergo misfolding and aggregation and accumulate in the extracellular space of their respective tissues of origin. As a main response to protein misfolding, there is evidence of the role of heat shock proteins (HSPs) in moderating T2D and AD. HSPs play a pivotal role in cell homeostasis by providing cytoprotection during acute and chronic metabolic stresses. In T2D and AD, intracellular HSP (iHSP) levels are reduced, potentially due to the ability of the cell to export HSPs to the extracellular space (eHSP). The increase in eHSPs can contribute to oxidative damage and is associated with various pro-inflammatory pathways in T2D and AD. Here, we review the role of HSP in moderating T2D and AD, as well as propose that these chaperone proteins are an important link in the relationship between T2D and AD.

DOI

10.3390/ijms21218204

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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