Effect of glucagon-like peptide-1 analogue; Exendin-4, on cognitive functions in type 2 diabetes mellitus; possible modulation of brain derived neurotrophic factor and brain Visfatin

Abdelwahed, Omaima Mohammed; Tork, Ola M.; Din, M.M. Gamal El; Rashed, Laila Ahmed; Zickri, Maha Baligh

doi:10.1016/j.brainresbull.2018.02.002

Cited by 24 publications

(12 citation statements)

References 79 publications

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“…Liraglutide could reverse deleterious effects of insulin resistance in neuronal cells by improving the phosphorylation status of insulin receptor, IRS-1 and Akt( Jantrapirom et al, 2020 ). Exendine-4, a long-acting GLP-1 receptor agonist, inhibited glucose-induced apoptosis and oxidative stress in neurons( Chen et al, 2012 ), and ameliorated cognitive impairment( Chen et al, 2012 ) involving its metabolic, anti-inflammatory and anti-oxidant effects( Solmaz et al, 2015 ; Abdelwahed et al, 2018 ). The activation of GLP-1 receptor could attenuate neuroinflammation and improve neurogenesis and insulin sensitivity in AD( Bae and Song, 2017 ).…”

Section: Repurposing Of Anti-diabetic Agents As a Potential Treatment Targeting Cognitive Function In Ad And Schizophreniamentioning

confidence: 99%

Repurposing of Anti-Diabetic Agents as a New Opportunity to Alleviate Cognitive Impairment in Neurodegenerative and Neuropsychiatric Disorders

Chen

Cao

et al. 2021

Front. Pharmacol.

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Cognitive impairment is a shared abnormality between type 2 diabetes mellitus (T2DM) and many neurodegenerative and neuropsychiatric disorders, such as Alzheimer’s disease (AD) and schizophrenia. Emerging evidence suggests that brain insulin resistance plays a significant role in cognitive deficits, which provides the possibility of anti-diabetic agents repositioning to alleviate cognitive deficits. Both preclinical and clinical studies have evaluated the potential cognitive enhancement effects of anti-diabetic agents targeting the insulin pathway. Repurposing of anti-diabetic agents is considered to be promising for cognitive deficits prevention or control in these neurodegenerative and neuropsychiatric disorders. This article reviewed the possible relationship between brain insulin resistance and cognitive deficits. In addition, promising therapeutic interventions, especially current advances in anti-diabetic agents targeting the insulin pathway to alleviate cognitive impairment in AD and schizophrenia were also summarized.

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Section: Repurposing Of Anti-diabetic Agents As a Potential Treatment Targeting Cognitive Function In Ad And Schizophreniamentioning

confidence: 99%

Repurposing of Anti-Diabetic Agents as a New Opportunity to Alleviate Cognitive Impairment in Neurodegenerative and Neuropsychiatric Disorders

Chen

Cao

et al. 2021

Front. Pharmacol.

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“…Moreover, studies focusing on brain derived neurotrophic factor (BDNF), one of the most essential neurotrophic factors in the brain [ 27 ], and dipeptidyl peptidase-4 (DPP4), initially identified as a therapeutic target for type 2 diabetes [ 28 ], have demonstrated that both BDNF and DPP4 function as an antigenic enzyme involved in hyperglycemia, oxidative stress and inflammation-associated insulin resistance [ 29 ]). These studies provide evidence for the role of increased DPP4 and decreased BDNF in type 2-DM-related cognitive dysfunction [ 30 ], suggesting that DPP4 to BDNF ratio could be a novel biomarker for DM-related cognitive impairment [ 31 ].…”

Section: Potential Mechanism In the Development Of Diabetic Cognitmentioning

confidence: 99%

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

Xing¹,

Tang²,

Lei³

et al. 2020

Aging and disease

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The goal of this review was to summarize current biochemical mechanisms of and risk factors for diabetic brain injury. We mainly summarized mechanisms published in the past three years and focused on diabetes induced cognitive impairment, diabetes-linked Alzheimer's disease, and diabetic stroke. We think there is a need to conduct further studies with increased sample sizes and prolonged period of follow-ups to clarify the effect of DM on brain dysfunction. Additionally, we also think that enhancing experimental reproducibility using animal models in conjunction with application of advanced devices should be considered when new experiments are designed. It is expected that further investigation of the underlying mechanisms of diabetic cognitive impairment will provide novel insights into therapeutic approaches for ameliorating diabetes-associated injury in the brain.

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“…injection and suggests that peripheral mediators may be needed for the action of α‐MSH on central BDNF expression. MC4R has been reported to be expressed in the gastrointestinal system, with its activation inducing glucagon‐like peptide 1 (GLP‐1) expression; an analogue of this hormone was shown to stimulate BDNF expression in the brain . Considering these data, GLP‐1 could be considered as a possible mediator of the melanocortin effect on hypothalamic BDNF expression.…”

Section: Discussionmentioning

confidence: 99%

NDP‐MSH reduces oxidative damage induced by palmitic acid in primary astrocytes

Ramírez

Saba

Turati

et al. 2019

J Neuroendocrinology

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Recent findings relate obesity to inflammation in key hypothalamic areas for body weight control. Hypothalamic inflammation has also been related to oxidative stress.Palmitic acid (PA) is the most abundant free fatty acid found in food, and in vitro studies indicate that it triggers a pro-inflammatory response in the brain.Melanocortins are neuropeptides with proven anti-inflammatory and neuroprotective action mediated by melanocortin receptor 4 (MC4R), but little is known about the effect of melanocortins on oxidative stress. The aim of this study was to investigate whether melanocortins could alleviate oxidative stress induced by a high fat diet (HFD) model. We found that NDP-MSH treatment decreased PA-induced reactive oxygen species production in astrocytes, an effect blocked by the MC4R inhibitor JKC363. NDP-MSH abolished nuclear translocation of Nrf2 induced by PA and blocked the inhibitory effect of PA on superoxide dismutase (SOD) activity and glutathione levels while it also per se increased activity of SOD and γ-glutamate cysteine ligase (γ-GCL) antioxidant enzymes. However, HFD reduced hypothalamic MC4R and brain derived neurotrophic factor mRNA levels, thereby preventing the neuroprotective mechanism induced by melanocortins. K E Y W O R D Sastrocytes, high-fat diet, MC4R, oxidative stress, palmitic acid

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Effect of glucagon-like peptide-1 analogue; Exendin-4, on cognitive functions in type 2 diabetes mellitus; possible modulation of brain derived neurotrophic factor and brain Visfatin

Cited by 24 publications

References 79 publications

Repurposing of Anti-Diabetic Agents as a New Opportunity to Alleviate Cognitive Impairment in Neurodegenerative and Neuropsychiatric Disorders

Repurposing of Anti-Diabetic Agents as a New Opportunity to Alleviate Cognitive Impairment in Neurodegenerative and Neuropsychiatric Disorders

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

NDP‐MSH reduces oxidative damage induced by palmitic acid in primary astrocytes

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