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Unraveling the molecular crossroads: T2DM and Parkinson’s disease interactions

TINGTING LIU#, XIANGRUI KONG#, JIANSHE WEI*
Institute for Brain Sciences Research, School of Life Sciences, Henan University, Kaifeng, 475004, China
* Corresponding Author: JIANSHE WEI. Email: email
# These two authors contributed equally to this work
(This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)

BIOCELL https://doi.org/10.32604/biocell.2024.056272

Received 18 July 2024; Accepted 27 September 2024; Published online 09 October 2024

Abstract

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by persistent hyperglycemia. In recent times, an elevated risk of Parkinson’s disease (PD) development among individuals with T2DM has become evident. However, the molecular mechanisms that underpin the interplay between T2DM and the pathogenesis of PD remain to be elucidated. Nevertheless, recent epidemiological studies have underscored several shared molecular pathways that are crucial for normal cellular function and are also associated with the progression and etiology of both T2DM and PD. This review encapsulates some of the shared pathophysiological mechanisms, including genetic risk factors, hyperglycemia, insulin resistance (IR), inflammation, mitochondrial dysfunction, oxidative stress, autophagy, and advanced glycation end products (AGEs), which independently contribute to the onset and progression of T2DM and PD. Additionally, this review compiles studies that have investigated the relationship between T2DM and PD. This review aims to offer insights into the overlapping molecular pathways involved, which may suggest alternative therapeutic strategies for both T2DM and PD.

Keywords

Type 2 diabetes mellitus; Parkinson’s disease; Oxidative stress; Mitochondrial dysfunction; Autophagy

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