Glibenclamide modulates microglial function and attenuates Aβ deposition in 5XFAD mice

Ju, Yeon-Joo; Kim, Namkwon; Gee, Min Sung; Jeon, Seung Ho; Lee, Danbi; Do, Jimin; Ryu, Jong-Sik; Lee, Jong Kil

doi:10.1016/j.ejphar.2020.173416

Cited by 10 publications

(7 citation statements)

References 37 publications

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“…In both BV2 microglial cells and mouse PD models, glibenclamide was able to limit microglial activation and reduce excessive neuroinflammation. Furthermore, glibenclamide’s anti-neuroinflammation actions may be caused through mechanisms that regulate the c-Jun N-terminal kinase (JNK) and NF-B signalling pathways [ 224 ]. Together, these data suggest a possible role of sulfonylureas in treating both PD and T2DM.…”

Section: Drugs Available For T2dmmentioning

confidence: 99%

Type 2 Diabetes (T2DM) and Parkinson’s Disease (PD): a Mechanistic Approach

et al. 2023

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Growing evidence suggest that there is a connection between Parkinson’s disease (PD) and insulin dysregulation in the brain, whilst the connection between PD and type 2 diabetes mellitus (T2DM) is still up for debate. Insulin is widely recognised to play a crucial role in neuronal survival and brain function; any changes in insulin metabolism and signalling in the central nervous system (CNS) can lead to the development of various brain disorders. There is accumulating evidence linking T2DM to PD and other neurodegenerative diseases. In fact, they have a lot in common patho-physiologically, including insulin dysregulation, oxidative stress resulting in mitochondrial dysfunction, microglial activation, and inflammation. As a result, initial research should focus on the role of insulin and its molecular mechanism in order to develop therapeutic outcomes. In this current review, we will look into the link between T2DM and PD, the function of insulin in the brain, and studies related to impact of insulin in causing T2DM and PD. Further, we have also highlighted the role of various insulin signalling pathway in both T2DM and PD. We have also suggested that T2DM-targeting pharmacological strategies as potential therapeutic approach for individuals with cognitive impairment, and we have demonstrated the effectiveness of T2DM-prescribed drugs through current PD treatment trials. In conclusion, this investigation would fill a research gap in T2DM-associated Parkinson’s disease (PD) with a potential therapy option. Graphical Abstract

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Section: Drugs Available For T2dmmentioning

confidence: 99%

Type 2 Diabetes (T2DM) and Parkinson’s Disease (PD): a Mechanistic Approach

et al. 2023

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“…Like other antidiabetic drugs, sulfonylureas are being investigated in the field of neurodegenerative diseases. In experimental AD, sulfonylureas improve memory and maintain synaptic plasticity, and inhibit acetylcholinesterase (Baraka and ElGhotny, 2010;Esmaeili et al, 2018;Ju et al, 2020;Salgado-Puga et al, 2017). When evaluating neuroinflammation, studies demonstrate that these drugs decrease microglia activation and levels of proinflammatory cytokines, TNF-α and IL-6, in the hippocampus of rodents undergoing experimental AD (Esmaeili et al, 2018;Ju et al, 2020).…”

Section: Sulfonylureasmentioning

confidence: 99%

“…In experimental AD, sulfonylureas improve memory and maintain synaptic plasticity, and inhibit acetylcholinesterase (Baraka and ElGhotny, 2010;Esmaeili et al, 2018;Ju et al, 2020;Salgado-Puga et al, 2017). When evaluating neuroinflammation, studies demonstrate that these drugs decrease microglia activation and levels of proinflammatory cytokines, TNF-α and IL-6, in the hippocampus of rodents undergoing experimental AD (Esmaeili et al, 2018;Ju et al, 2020). In a case control study, Imfeld et al (2012) showed that the long term use of sulfonylureas was not associated with an altered risk for AD development.…”

Section: Sulfonylureasmentioning

confidence: 99%

Repositioning and development of new treatments for neurodegenerative diseases: Focus on neuroinflammation

Arbo

Schimith

Santos

et al. 2022

European Journal of Pharmacology

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“…The sulfonylurea family modulate ATP-sensitive potassium channels, which are involved in Ab-induced pathology. 19 In this context, glibenclamide treatment has been shown to reduce affective disorders, 20 memory impairment and neuroinflammation 21 as well as Ab deposition 22 in different rodent models of AD.…”

Section: (Esi †)mentioning

confidence: 99%