Bilateral quinolinic acid-induced lipid peroxidation, decreased striatal monoamine levels and neurobehavioral deficits are ameliorated by GIP receptor agonist D-Ala 2 GIP in rat model of Huntington's disease

Verma, Mahip K.; Goel, Rajan; Nandakumar, Krishnadas; Nemmani, Kumar V.S.

doi:10.1016/j.ejphar.2018.03.034

Cited by 15 publications

(4 citation statements)

References 60 publications

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“…LPO levels are based on the detection of MDA and 4-HNE, which have strong mutagenicity and cytotoxicity [ 27 ]. In animal experiments, Verma et al demonstrated that the reduction of lipid peroxidation is an important reason to relieve abnormal behavior in the QA-induced HD model [ 28 ], and data from Lee et al showed that the modulation of lipid peroxidation and mitochondrial function improves neuropathology in HD mice [ 29 ]. Additionally, Skouta et al suggested that lipid peroxidation mediates Huntington's disease phenotypes and found that the drug inhibited oxidative lipid peroxidation and reduced cell death in cellular models of Huntington's disease (HD) [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Blood Oxidative Stress Marker Aberrations in Patients with Huntington’s Disease: A Meta-Analysis Study

Tang

Liu

Xiao

et al. 2020

Oxidative Medicine and Cellular Longevity

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Huntington’s disease (HD) is a hereditary autosomal dominant neurodegenerative disease. Although studies have shown that blood oxidative stress markers are dysregulated in HD patients, clinical data on the blood oxidative stress markers of HD patients is inconsistent. To better understand the pathogenesis of HD, we performed a systematic review and meta-analysis of blood oxidative stress markers in HD patients and healthy control (HC) subjects. A database search from PubMed and Web of Science identified 12 studies with 375 HD patients and 447 HC subjects in this meta-analysis. A random-effects meta-analysis showed that blood lipid peroxidation products (Hedges’ g=0.883, 95%CI=0.637 to 1.130, p<0.001), 8-hydroxyguanosine (Hedges’ g=1.727, 95%CI=0.489 to 2.965, p=0.006) levels, and the activity of glutathione peroxidase (Hedges’ g=2.026, 95%CI=0.570 to 3.482, p=0.006) were significantly increased in HD patients compared to controls. In contrast, reduced glutathione levels were lower in HD patients than in controls (Hedges’ g=−0.611, 95%CI=−1.016 to−0.207, p=0.003). However, blood superoxide dismutase, cholesterol, high-density lipoproteins, low-density lipoproteins, and triglycerides did not show significant differences between cases and controls. Taken together, this study clarified the associations between blood oxidative stress markers and HD, supporting the clinical evidence that HD is accompanied by increased oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Blood Oxidative Stress Marker Aberrations in Patients with Huntington’s Disease: A Meta-Analysis Study

Tang

Liu

Xiao

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Therefore, the second aim in this study was to evaluate the usefulness of a neurological examination of sheep for diagnosing and characterizing the phenotype of sheep with quinolinic acid (QA) lesions of the striatum. QA is an excitotoxin that has been used extensively in rats [25][26][27][28][29], mice [30,31], and non-human primates [23,32,33] to lesion the striatum and create an acute toxic model of HD.…”

Section: Chemicals and Surgical Methodsmentioning

confidence: 99%

Neurological Examination of Sheep (Ovis aries) with Unilateral and Bilateral Quinolinic Acid Lesions of the Striatum Assessed by Magnetic Resonance Imaging

O'Connell¹,

Sinnott²,

Kuchel³

et al. 2019

J Neurol Exp Neurosci

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Acute toxic models of Huntington's disease (HD) and Parkinson's disease (PD) have been used extensively to study neuropathology and behavior in rodents and non-human primates, but not large animals. We have created an acute quinolinic acid (QA) model of HD in sheep (Ovis aries), first to investigate the clinical signs of ovine striatum pathology and second to assess the value of a veterinary neurological examination in the symptomology investigation. Sixteen sheep underwent two surgeries, four weeks apart, in which either QA or saline was infused into the left (unilateral) and then the right (bilateral) caudate nucleus. Neurological examinations were performed pre-surgically, two weeks after the unilateral surgery and eight weeks after the bilateral surgery. Examining veterinarians were blind to treatment group. Evidence of laterality and hind limb motor dysfunction was identified in the QA-lesioned sheep. The neurological examination identified clinical signs in two out of eight saline control sheep and four out of eight QA-lesioned sheep after the unilateral surgery and three out of eight saline control sheep and seven out of eight QA-lesioned sheep after the bilateral lesion surgery. There was no association between clinical profile and treatment group, or lesion size and location. While the neurological examination was moderately useful for identification of QA-lesioned sheep, it was not informative about lesion characteristics.

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“…Furthermore, in the HD brain slice model, a method that decreased the peroxidation of lipids with ferritin 1 minimized cellular death (Skouta et al, 2014 ). Similarly, glucose-dependent insulin stimulation of the polypeptide (GiP) receptor D-Ala 2GiP and deuterium-enhanced linoleic acid ameliorated neurobehavioral deficits and attenuated cognitive deficits in HD patients by reducing lipid peroxidation (Hatami et al, 2018 ; Verma et al, 2018 ). Heat shock protein 27 (HSP27) reduces ROS in expressing mHtt cells and protects cells from oxidative stress.…”

Section: Pathologic Relationship Between Ferroptosis and Neurodegener...mentioning

confidence: 99%

Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases

Wang,

Fang,

Ling

et al. 2024

Front. Cell. Neurosci.

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Globally, millions of individuals are impacted by neurodegenerative disorders including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD). Although a great deal of energy and financial resources have been invested in disease-related research, breakthroughs in therapeutic approaches remain elusive. The breakdown of cells usually happens together with the onset of neurodegenerative diseases. However, the mechanism that triggers neuronal loss is unknown. Lipid peroxidation, which is iron-dependent, causes a specific type of cell death called ferroptosis, and there is evidence its involvement in the pathogenic cascade of neurodegenerative diseases. However, the specific mechanisms are still not well known. The present article highlights the basic processes that underlie ferroptosis and the corresponding signaling networks. Furthermore, it provides an overview and discussion of current research on the role of ferroptosis across a variety of neurodegenerative conditions.

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Bilateral quinolinic acid-induced lipid peroxidation, decreased striatal monoamine levels and neurobehavioral deficits are ameliorated by GIP receptor agonist D-Ala 2 GIP in rat model of Huntington's disease

Cited by 15 publications

References 60 publications

Blood Oxidative Stress Marker Aberrations in Patients with Huntington’s Disease: A Meta-Analysis Study

Blood Oxidative Stress Marker Aberrations in Patients with Huntington’s Disease: A Meta-Analysis Study

Neurological Examination of Sheep (Ovis aries) with Unilateral and Bilateral Quinolinic Acid Lesions of the Striatum Assessed by Magnetic Resonance Imaging

Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases

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