Physiological Targets for the Treatment of Diabetic Encephalopathy

Vieira, Lucas Lima; Soares, Rafaela de Lima Gomes; Felipe, Stela Mirla da Silva; Moura, Felipe Carmo de; Brito, Gerly Anne de Castro; Pacheco, Christina; Soares, Paula Matias

doi:10.2174/1871524916666160428111015

Cited by 11 publications

(8 citation statements)

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“…Diabetic encephalopathy involves direct neuronal damage caused by persistent hyperglycemia, a phenomenon referred to as glucose neurotoxicity (1, 3). However, the pathogenesis of this disease is poorly understood and its diagnosis is complicated due to multiple pathogenic pathways involved (4, 5). Cognitive impairment is one of the many consequences of such toxicity that reduces the quality of life of patients (6–9).…”

Section: Introductionmentioning

confidence: 99%

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

et al. 2019

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Diabetic encephalopathy is a severe diabetes-related complication in the central nervous system (CNS) that is characterized by degenerative neurochemical and structural changes leading to impaired cognitive function. While the exact pathophysiology of diabetic encephalopathy is not well-understood, it is likely that neuroinflammation is one of the key pathogenic mechanisms that cause this complication. Lipocalin-2 (LCN2) is an acute phase protein known to promote neuroinflammation via the recruitment and activation of immune cells and glia, particularly microglia and astrocytes, thereby inducing proinflammatory mediators in a range of neurological disorders. In this study, we investigated the role of LCN2 in multiple aspects of diabetic encephalopathy in mouse models of diabetes. Here, we show that induction of diabetes increased the expression of both Lcn2 mRNA and protein in the hippocampus. Genetic deficiency of Lcn2 significantly reduced gliosis, recruitment of macrophages, and production of inflammatory cytokines in the diabetic mice. Further, diabetes-induced hippocampal toxicity and cognitive decline were both lower in Lcn2 knockout mice than in the wild-type animals. Taken together, our findings highlight the critical role of LCN2 in the pathogenesis of diabetic encephalopathy.

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Section: Introductionmentioning

confidence: 99%

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

et al. 2019

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“…The mechanisms underlying diabetic encephalopathy had been believed to be relevant with vascular amylin deposition [ 8 ], oxidative and nitrative stress [ 9 ], inflammation, hyperglycemic internal environment [ 10 , 11 ], endoplasmic reticulum (ER) stress, autophagy defects, and immune receptors [ 12 ]. Wang, Z found that the inflammatory response related proteins were significantly increased in the brain with diabetes, including tumor necrosis factor-α (TNF-α), NF-κB, cyclooxygenase-2 (Cox-2) and interleukin-6 (IL-6) [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Curcumin and its analog alleviate diabetes-induced damages by regulating inflammation and oxidative stress in brain of diabetic rats

Miao

Chen

et al. 2021

Diabetol Metab Syndr

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Background Diabetic encephalopathy is a severe diabetes complication with cognitive dysfunction and neuropsychiatric disability. The mechanisms underlying diabetic encephalopathy is believed to be relevant with oxidative stress, vascular amylin deposition, immune receptors, inflammation, etc. This study wanted to evaluate the ability of curcumin and its analog A13 to alleviate oxidative stress and inflammation in diabetes-induced damages in brain. Methods Sixty adult male Sprague–Dawley rats were divided into 5 groups: normal control (NC) group, diabetes mellitus (DM) group, curcumin-treated diabetes mellitus (CUR) group, high dose of A13-treated diabetes mellitus (HA) group, low dose of A13-treated diabetes mellitus (LA) group. Activation of the nuclear factor kappa-B (NF-κB p65) pathway was detected by RT-qPCR, immunohistochemical (IHC) staining and Western blot; oxidative stress was detected by biochemical detection kit; brain tissue sections were stained with hematoxylin–eosin (HE) staining and Myelin staining. Results RT-qPCR, IHC staining and Western blot showed that curcumin and A13 treatment could inhibit the NF-κB p65 pathway. Curcumin and A13 increased the activity of superoxide dismutase and decreased the malondialdehyde level in the brain of diabetic rats. Furthermore, HE staining and Myelin staining demonstrated that the histological lesions of the brain in diabetic rats could be significantly ameliorated by curcumin and A13. Conclusion Curcumin analog A13 could alleviate the damages in the brain of diabetes rats by regulating the pathways of inflammation and oxidative stress. A13 may be a new potential therapeutic agent for diabetic encephalopathy.

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“…На сегодняшний день для коррекции когнитивных нарушений при СД в основном используются антигипоксанты [22][23][24][25][26]. Кроме того, применение медикаментозной терапии, улучшающей когнитивные функции при умеренных когнитивных нарушениях, в настоящее время не имеет доказательной базы [27,28].…”

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Perspectives for cognitive rehabilitation of patients with diabetes mellitus

et al. 2016

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Currently, the problem of cognitive dysfunction is becoming increasingly important due to the raising demand for effective intellectual activity in modern society. One of the most significant causes of cognitive dysfunction is dismetabolic nature of the disorder, such as diabetes mellitus, which has recently been gaining prevalence. Much of the resistance of clinical symptoms of diabetic encephalopathy to conventional therapy requires a search for new approaches for solving this problem. Cognitive rehabilitation as a correctional technique has proved a positive effect in terms of the treatment of neurodegenerative diseases of different nature.This review present the ways for correction of cognitive impairment using the method of cognitive rehabilitation in patients with diabetes, its methodology, mechanisms of action and perspectives.

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Physiological Targets for the Treatment of Diabetic Encephalopathy

Cited by 11 publications

References 0 publications

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

Curcumin and its analog alleviate diabetes-induced damages by regulating inflammation and oxidative stress in brain of diabetic rats

Perspectives for cognitive rehabilitation of patients with diabetes mellitus

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