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. 2024 Nov 5;31:102. doi: 10.1186/s12929-024-01090-x

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — The postulated mechanism by which diabetes contributes to neurodegeneration in Alzheimer’s disease (AD) and Parkinson’s disease (PD) may involve the accumulation of advanced glycation end products (AGE) and cellular insulin resistance (IR). For the target organ, brain, these two phenomenon lead to inflammation, vascular occlusion, oxidative stress, and the aggregation of pathognomonic proteins, which, in turn, trigger neurodegeneration in the cerebral cortex for dementia, such as AD and vascular dementia (VaD), and the substantia nigra for parkinsonism, such as PD and vascular parkinsonism (VaP)