Category: Moms

Oxidative stress and neurodegenerative diseases

Oxidative stress and neurodegenerative diseases

Oxieative, J. Neurdegenerative 19, Current Diabetes Reviews. The Lowering cholesterol with medication limiting membrane Oxidative stress and neurodegenerative diseases from astrocytes creates a barrier between Oxidative stress and neurodegenerative diseases brain parenchyma and the vascular system Ransom et al. In this respect, it has been found that the mobilization of T cells with anti-inflammatory characteristics toward damaged regions of the CNS can provide neuroprotection and become a therapeutic strategy to control inflammatory processes in neurodegeneration.

Oxidative stress and neurodegenerative diseases -

Most such drugs have so far failed to slow down the progression of the disease or to prolong the lives of patients. Some exceptions within these anti-neurodegenerative drugs exist, and they give hope and inspire further research. Li J, O W, Li W, Jiang Z, Ghanbari HA Oxidative stress and neurodegenerative disorders.

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Hum Mol Genet R—R Corcia P, Blasco H, Camu W Genetics of amyotrophic lateral sclerosis. Presse Med — Mendez EF, Sattler R Biomarker development for C9orf72 repeat expansion in ALS.

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Neuron — Rakhit R, Crow JP, Lepock JR, Kondejewski LH, Cashman NR, Chakrabartty A Monomeric Cu, Zn-superoxide dismutase is a common misfolding intermediate in the oxidation models of sporadic and familial amyotrophic lateral sclerosis.

J Biol Chem — Ezzi SA, Urushitani M, Julien J Wild-type superoxide dismutase acquires binding and toxic properties of ALS-linked mutant forms through oxidation.

J Neurochem — Ito H, Wate R, Zhang J, Ohnishi S, Kaneko S, Ito H, Nakano S, Kusaka H Treatment with edaravone, initiated at symptom onset, slows motor decline and decreases SOD1 deposition in ALS mice. Exp Neurol — Watanabe M, Dykes-Hoberg M, Cizewski Culotta V, Price DL, Wong PC, Rothstein JD Histological evidence of protein aggregation in mutant SOD1 transgenic mice and in amyotrophic lateral sclerosis neural tissues.

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PLoS ONE 5. Tohgi H, Abe T, Yamizaki K, Murata T, Ishizaki E, Isobe C Remarkable increase in cerebrospinal fluid 3-nitrotyrosine in patients with sporadic amyotrophic lateral sclerosis.

Ann Neurol — Smith RG, Henry YK, Mattson MP, Appel SH Presence of 4-hydroxynonenal in cerebrospinal fluid of patients with sporadic amyotrophic lateral sclerosis.

Ihara Y, Nobukuni K, Takata H, Hayabara T Oxidative stress and metal content in blood and cerebrospinal fluid of amyotrophic lateral sclerosis patients with and without a Cu, Zn-superoxide dismutase mutation.

Neurol Res — Barber SC, Shaw PJ Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. Oteiza PI, Uchitel OD, Carrasquedo F, Dubrovski AL, Roma JC, Fraga CG Evaluation of antioxidants, protein, and lipid oxidation products in blood from sporadic amiotrophic lateral sclerosis patients.

Neurochem Res — Babu GN, Kumar A, Chandra R, Puri SK, Singh RL, Kalita J, Misra UK Oxidant-antioxidant imbalance in the erythrocytes of sporadic amyotrophic lateral sclerosis patients correlates with the progression of disease. Neurochem Int — LoGerfo A, Chico L, Borgia L, et al.

Oxidat Med Cell Longevity, vol. doi: Mitsumoto H, Santella R, Liu X, Bogdanov M, Zipprich J, Wu H, Mahata J, Kilty M, Bednarz K, Bell D, Gordon PH, Hornig M, Mehrazin M, Naini A, Flint Beal M, Factor-Litvak P Oxidative stress biomarkers in sporadic ALS. Amyotrophic Lat Scler — Ikawa M, Okazawa H, Tsujikawa T, Muramatsu T, Kishitani T, Kamisawa T, Matsunaga A, Yamamura O, Mori T, Hamano T, Kiyono Y, Nakamoto Y, Yoneda M Increased cerebral oxidative stress in amyotrophic lateral sclerosis: a 62CU-ATSM pet study.

Neurology Tohgi H, Abe T, Yamazaki K, Murata T, Ishizaki E, Isobe C Increase in oxidized NO products and reduction in oxidized glutathione in cerebrospinal fluid from patients with sporadic form of amyotrophic lateral sclerosis.

Boll M, Alcaraz-Zubeldia M, Montes S, Murillo-Bonilla L, Rios C Raised nitrate concentration and low SOD activity in the CSF of sporadic ALS patients. Nikolic-Kokic A, Stevic Z, Blagojevic D, Davidovic B, Jones DR, Spasic MB Alterations in anti-oxidative defence enzymes in erythrocytes from sporadic amyotrophic lateral sclerosis SALS and familial ALS patients.

Clin Chem Lab Med — Apostolski S, Marinkovic Z, Nikolic A, Blagojevic D, Spasic MB, Michael Michelson A Glutathione peroxidase in amyotrophic lateral sclerosis: the effects of selenium supplementation.

J Environ Pathol Toxicol Oncol — Kokic AN, Stevic Z, Stojanovic S, Blagojevic DP, Jones DR, Pavlovic S, Niketic V, Apostolski S, Spasic MB Biotransformation of nitric oxide in the cerebrospinal fluid of amyotrophic lateral sclerosis patients. Redox Rep — Süssmuth SD, Brettschneider J, Ludolph AC, Tumani H Biochemical markers in CSF of ALS patients.

Curr Med Chem — Tanaka H, Shimazawa M, Takata M, Kaneko H, Tsuruma K, Ikeda T, Warita H, Aoki M, Yamada M, Takahashi H, Hozumi I, Minatsu H, Inuzuka T, Hara H ITIH4 and Gpx3 are potential biomarkers for amyotrophic lateral sclerosis.

J Neurol — Kuzma M, Jamrozik Z, Baranczyk-Kuzma A Activity and expression of glutathione S-transferase pi in patients with amyotrophic lateral sclerosis.

Clin Chim Acta — Cova E, Bongioanni P, Cereda C, Metelli MR, Salvaneschi L, Bernuzzi S, Guareschi S, Rossi B, Ceroni M Time course of oxidant markers and antioxidant defenses in subgroups of amyotrophic lateral sclerosis patients.

De Bustos F, Jiménez-Jiménez FJ, Molina JA, Esteban J, Guerrero-Sola A, Zurdo M, Ortì-Pareja M, Tallón-Barranco A, Gómez-Escalonilla C, Ramírez-Ramos C, Arenas J, Enríquez De Salamanca R Cerebrospinal fluid levels of alpha-tocopherol in amyotrophic lateral sclerosis.

J Neural Transm — Acta Neurol Scand — Johnson WM, Wilson-Delfosse AL, Mieyal JJ Dysregulation of glutathione homeostasis in neurodegenerative diseases. Nutrients — Desnuelle C, Dib M, Garrel C, Favier A A double-blind, placeho-controlled randomized clinical trial of a-tocopherol vitamin E in the treatment of amyotrophic lateral sclerosis.

Amyotrop Lateral Sclerosis Motor Neuron Disord — Graf M, Ecker D, Horowski R, Kramer B, Riederer P, Gerlach M, Hager C, Ludolph AC High dose vitamin E therapy in amyotrophic lateral sclerosis as add-on therapy to riluzole: results of a placebo-controlled double-blind study. Veldink JH, Kalmijn S, Groeneveld G, Wunderink W, Koster A, De Vries JHM, Van Der Luyt J, Wokke JHJ, Van Den Berg LH Intake of polyunsaturated fatty acids and vitamin E reduces the risk of developing amyotrophic lateral sclerosis.

J Neurol Neurosurg Psychiatry — Yoshino H, Kimura A Investigation of the therapeutic effects of edaravone, a free radical scavenger, on amyotrophic lateral sclerosis phase II study.

Amyotrop Later Sclerosis: Off Public World Fed Neurol Res Group Motor Neuron Dis — Accessed 15 May Kaufmann P, Thompson JLP, Levy G, Buchsbaum R, Shefner J, Krivickas LS, Katz J, Rollins Y, Barohn RJ, Jackson CE, Tiryaki E, Lomen-Hoerth C, Armon C, Tandan R, Rudnicki SA, Rezania K, Sufit R, Pestronk A, Novella SP, Heiman-Patterson T, Kasarskis EJ, Pioro EP, Montes J, Arbing R, Vecchio D, Barsdorf A, Mitsumoto H, Levin B Phase II trial of CoQ10 for ALS finds insufficient evidence to justify phase III.

Groeneveld GJ, Veldink JH, Van der Tweel I, Kalmijn S, Beijer C, De Visser M, Wokke JHJ, Franssen H, Van den Berg LH A randomized sequential trial of creatine in amyotrophic lateral sclerosis.

Louwerse ES, Weverling GJ, Bossuyt PMM, Meyjes FEP, De Jong JMBV Randomized, double-blind, controlled trial of acetylcysteine in amyotrophic lateral sclerosis. Arch Neurol — Lange DJ, Murphy PL, Diamond B, Appel V, Lai EC, Younger DS, Appel SH Selegiline is ineffective in a collaborative double-blind, placebo-controlled trial for treatment of amyotrophic lateral sclerosis.

Weishaupt JH, Bartels C, Pölking E, Dietrich J, Rohde G, Poeggeler B, Mertens N, Sperling S, Bohn M, Hüther G, Schneider A, Bach A, Sirén A, Hardeland R, Bähr M, Nave K, Ehrenreich H Reduced oxidative damage in ALS by high-dose enteral melatonin treatment.

J Pineal Res — Zoccolella S. Lamberti, P. Neuropsychiat Dis Treatment Vol 5, Issue 1, , Pages — — Turner BJ, Talbot K Transgenics, toxicity and therapeutics in rodent models of mutant SOD1-mediated familial ALS.

McGoldrick P, Joyce PI, Fisher EMC, Greensmith L Rodent models of amyotrophic lateral sclerosis. Biochim Biophys Acta BBA - Mol Basis Dis — Liu D, Wen J, Liu J, Li L The roles of free radicals in amyotrophic lateral sclerosis: reactive oxygen species and elevated oxidation of protein, DNA, and membrane phospholipids.

FASEB J — Towner RA, Smith N, Saunders D, Lupu F, Silasi-Mansat R, West M, Ramirez DC, Gomez-Mejiba SE, Bonini MG, Mason RP, Ehrenshaft M, Hensley K In vivo detection of free radicals using molecular MRI and immuno-spin trapping in a mouse model for amyotrophic lateral sclerosis.

Poon HF, Hensley K, Thongboonkerd V, Merchant ML, Lynn BC, Pierce WM, Klein JB, Calabrese V, Butterfield DA Redox proteomics analysis of oxidatively modified proteins in G93A-SOD1 transgenic mice—a model of familial amyotrophic lateral sclerosis. Liu D, Bao F, Wen J, Liu J Mutation of superoxide dismutase elevates reactive species: comparison of nitration and oxidation of proteins in different brain regions of transgenic mice with amyotrophic lateral sclerosis.

Neuroscience — Miana-Mena FJ, González-Mingot C, Larrodé P, Muñoz MJ, Oliván S, Fuentes-Broto L, Martínez-Ballarín E, Reiter RJ, Osta R, García JJ Monitoring systemic oxidative stress in an animal model of amyotrophic lateral sclerosis.

Morimoto N, Miyazaki K, Kurata T, Ikeda Y, Matsuura T, Kang D, Ide T, Abe K Effect of mitochondrial transcription factor a overexpression on motor neurons in amyotrophic lateral sclerosis model mice. J Neurosci Res — Seo J, Baek I, Leem Y, Kim T, Cho Y, Lee SM, Park YH, Han P SK-PC-B70M alleviates neurologic symptoms in G93A-SOD1 amyotrophic lateral sclerosis mice.

Casoni F, Basso M, Massignan T, Gianazzail E, Cheroni C, Salmona M, Bendotti C, Bonetto V Protein nitration in a mouse model of familial amyotrophic lateral sclerosis: possible multifunctional role in the pathogenesis. Nardo G, Pozzi S, Mantovani S, Garbelli S, Marinou K, Basso M, Mora G, Bendotti C, Bonetto V Nitroproteomics of peripheral blood mononuclear cells from patients and a rat model of ALS.

PLoS ONE 4. Tokuda E, Ono S, Ishige K, Watanabe S, Okawa E, Ito Y, Suzuki T Ammonium tetrathiomolybdate delays onset, prolongs survival, and slows progression of disease in a mouse model for amyotrophic lateral sclerosis.

Chi L, Ke Y, Luo C, Gozal D, Liu R Depletion of reduced glutathione enhances motor neuron degeneration in vitro and in vivo. Vargas MR, Johnson DA, Johnson JA Decreased glutathione accelerates neurological deficit and mitochondrial pathology in familial ALS-linked hSOD1G93A mice model.

Vargas MR, Johnson DA, Sirkis DW, Messing A, Johnson JA Nrf2 activation in astrocytes protects against neurodegeneration in mouse models of familial amyotrophic lateral sclerosis. J Neurosci — Kato S, Kato M, Abe Y, Matsumura T, Nishino T, Aoki M, Itoyama Y, Asayama K, Awaya A, Hirano A, Ohama E Redox system expression in the motor neurons in amyotrophic lateral sclerosis ALS : immunohistochemical studies on sporadic ALS, superoxide dismutase 1 SOD1 -mutated familial ALS, and SOD1-mutated ALS animal models.

Kato S, Saeki Y, Aoki M, Nagai M, Ishigaki A, Itoyama Y, Kato M, Asayama K, Awaya A, Hirano A, Ohama E Histological evidence of redox system breakdown caused by superoxide dismutase 1 SOD1 aggregation is common to SOD1-mutated neurons in humans and animal models.

Cudkowicz ME, Pastusza KA, Sapp PC, Mathews RK, Leahy J, Pasinelli P, Francis JW, Jiang D, Andersen JK, Brown RH Jr Survival in transgenic ALS mice does not vary with CNS glutathione peroxidase activity.

Neurology — PLoS ONE 8. Klivenyi P, Kiaei M, Gardian G, Calingasan NY, Beal MF Additive neuroprotective effects of creatine and cyclooxygenase 2 inhibitors in a transgenic mouse model of amyotrophic lateral sclerosis.

Peña-Altamira E, Crochemore C, Virgili M, Contestabile A Neurochemical correlates of differential neuroprotection by long-term dietary creatine supplementation. Zhang W, Narayanan M, Friedlander RM Additive neuroprotective effects of minocycline with creatine in a mouse model of ALS.

Matthews RT, Ferrante RJ, Klivenyi P, Yang L, Klein AM, Mueller G, Kaddurah-Daouk R, Beal MF Creatine and cyclocreatine attenuate MPTP neurotoxicity.

Klivenyi P, Ferrante RJ, Matthews RT, Bogdanov MB, Klein AM, Andreassen OA, Mueller G, Wermer M, Kaddurah-Daouk R, Beal MF Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis.

Nat Med — Choi J, Küstermann E, Dedeoglu A, Jenkins BG Magnetic resonance spectroscopy of regional brain metabolite markers in FALS mice and the effects of dietary creatine supplementation. Eur J Neurosci — Derave W, Van Den Bosch L, Lemmens G, Eijnde BO, Robberecht W, Hespel P Skeletal muscle properties in a transgenic mouse model for amyotrophic lateral sclerosis: effects of creatine treatment.

Levkovitch-Verbin H, Waserzoog Y, Vander S, Makarovsky D, Piven I Minocycline upregulates pro-survival genes and downregulates pro-apoptotic genes in experimental glaucoma. Graefes Arch Clin Exp Ophthalmol — Chang Y, Kong Q, Shan X, Tian G, Ilieva H, Cleveland DW, Rothstein JD, Borchelt DR, Wong PC, Lin C-G Messenger RNA oxidation occurs early in disease pathogenesis and promotes motor neuron degeneration in ALS.

PLoS ONE 3. Tokuda E, Okawa E, Watanabe S, Ono S, Marklund SL Dysregulation of intracellular copper homeostasis is common to transgenic mice expressing human mutant superoxide dismutase-1s regardless of their copper-binding abilities.

Song L, Chen L, Zhang X, Li J, Le W Resveratrol ameliorates motor neuron degeneration and improves survival in SOD1G93A mouse model of amyotrophic lateral sclerosis.

BioMed Rese Int Dardiotis E, Panayiotou E, Feldman ML, Hadjisavvas A, Malas S, Vonta I, Hadjigeorgiou G, Kyriakou K, Kyriakides T Intraperitoneal melatonin is not neuroprotective in the G93ASOD1 transgenic mouse model of familial ALS and may exacerbate neurodegeneration.

Crow JP, Calingasan NY, Chen J, Hill JL, Beal MF Manganese porphyrin given at symptom onset markedly extends survival of ALS mice. Gurney ME, Cutting FB, Zhai P, Doble A, Taylor CP, Andrus PK, Hall ED Benefit of vitamin E, riluzole, and gabapentin in a transgenic model of familial amyotrophic lateral sclerosis.

Snow RJ, Turnbull J, Da Silva S, Jiang F, Tarnopolsky MA Creatine supplementation and riluzole treatment provide similar beneficial effects in copper, zinc superoxide dismutase G93A transgenic mice.

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Oxid Med Cell Longev Castellani RJ, Perry G, Siedlak SL, Nunomura A, Shimohama S, Zhang J, Montine T, Sayre LM, Smith MA Hydroxynonenal adducts indicate a role for lipid peroxidation in neocortical and brainstem Lewy bodies in humans.

Shamoto-Nagai M, Maruyama W, Hashizume Y, Yoshida M, Osawa T, Riederer P, Naoi M In parkinsonian substantia nigra, a-synuclein is modified by acrolein, a lipid-peroxidation product, and accumulates in the dopamine neurons with inhibition of proteasome activity.

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Mol Cell Neurosci — Ogata M, Kaneya D, Shin-Ya K, Li L, Abe Y, Katoh H, Seki S, Seki Y, Gonda R, Urano S, Endo T Trapping effect of eugenol on hydroxyl radicals induced by L-DOPA in vitro. Chem Pharm Bull — J Neuropathol Exp Neurol — Am J Pathol — Alam ZI, Jenner A, Daniel SE, Lees AJ, Cairns N, Marsden CD, Jenner P, Halliwell B Oxidative DNA damage in the Parkinsonian brain: an apparent selective increase in 8-hydroxyguanine levels in substantia nigra.

Boll M, Alcaraz-Zubeldia M, Montes S, Rios C Free copper, ferroxidase and SOD1 activities, lipid peroxidation and NOx content in the CSF. A different marker profile in four neurodegenerative diseases. Funct Neurol — Int J Neurosci — Sanders LH, Timothy Greenamyre J Oxidative damage to macromolecules in human Parkinson disease and the rotenone model.

Sato S, Mizuno Y, Hattori N Urinary 8-hydroxydeoxyguanosine levels as a biomarker for progression of Parkinson disease. Seet RCS, Lee CJ, Lim ECH, Tan JJH, Quek AML, Chong W, Looi W, Huang S, Wang H, Chan Y, Halliwell B Oxidative damage in Parkinson disease: measurement using accurate biomarkers.

Mov Disord — Connolly J, Siderowf A, Clark CM, Mu D, Pratico D F2 isoprostane levels in plasma and urine do not support increased lipid peroxidation in cognitively impaired parkinson disease patients. Cogn Behav Neurol — Riederer P, Sofic E, Rausch W, Schmidt B, Reynolds GP, Jellinger K, Youdim MBH Transition metals, ferritin, glutathione, and ascorbic acid in parkinsonian brains.

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Storch A, Jost WH, Vieregge P, Spiegel J, Greulich W, Durner J, MüLler T, Kupsch A, Henningsen H, Oertel WH, Fuchs G, Kuhn W, Niklowitz P, Koch R, Herting B, Reichmann H Randomized, double-blind, placebo-controlled trial on symptomatic effects of coenzyme Q10 in Parkinson disease.

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Acta Physiol Scandinav, Suppl — Langston JW, Forno LS, Rebert CS, Irwin I Selective nigral toxicity after systemic administration of 1-methylphenyl-1,2,5,6-tetrahydropyrine MPTP in the squirrel monkey. Blesa J, Juri C, Collantes M, Peñuelas I, Prieto E, Iglesias E, Martí-Climent J, Arbizu J, Zubieta JL, Rodríguez-Oroz MC, García-García D, Richter JA, Cavada C, Obeso JA Progression of dopaminergic depletion in a model of MPTP-induced parkinsonism in non-human primates.

An 18F-DOPA and 11C-DTBZ PET study. Neurosci Lett 1—2 — Jun 19; 1—2 —7. Epub Apr 3. Nat Neurosci — McCormack AL, Atienza JG, Johnston LC, Andersen JK, Vu S, Di Monte DA Role of oxidative stress in paraquat-induced dopaminergic cell degeneration.

Mol Neurobiol. Haleagrahara N, Siew CJ, Ponnusamy K Effect of quercetin and desferrioxamine on 6-hydroxydopamine 6-OHDA induced neurotoxicity in striatum of rats.

J Toxicol Sci — Eur Neuropsychopharmacol S Inden M, Kitamura Y, Kondo J, Hayashi K, Yanagida T, Takata K, Tsuchiya D, Yanagisawa D, Nishimura K, Taniguchi T, Shimohama S, Sugimoto H, Akaike A Serofendic acid prevents 6-hydroxydopamine-induced nigral neurodegeneration and drug-induced rotational asymmetry in hemi-parkinsonian rats.

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Acta Pharmacol Sin — J Neuroinflammat 9. Neurotoxicology — Pharmacol Biochem Behav — Liang L, Huang J, Fulton R, Day BJ, Patel M An orally active catalytic metalloporphyrin protects against 1-methylphenyl-1,2,3,6-tetrahydropyridine neurotoxicity in vivo. Ahmad M, Saleem S, Ahmad AS, Yousuf S, Ansari MA, Khan MB, Ishrat T, Chaturvedi RK, Agrawal AK, Islam F Ginkgo biloba affords dose-dependent protection against 6-hydroxydopamine-induced parkinsonism in rats: neurobehavioural, neurochemical and immunohistochemical evidences.

Thomas B, Mohanakumar KP Melatonin protects against oxidative stress caused by 1-methylphenyl-1, 2,3,6-tetrahydropyridine in the mouse nigrostriatum.

Neurotoxicity Res. Chen C, Yin M, Hsu C, Liu T Antioxidative and anti-inflammatory effects of four cysteine-containing agents in striatum of MPTP-treated mice. Nutrition — J Neurol Sci Sharma A, Kaur P, Kumar V, Gill KD Attenuation of 1-methylphenyl-1,2,3,6-tetrahydropyridine induced nigrostriatal toxicity in mice by N-acetyl cysteine.

Cell Mol Biol — Ansari MA, Scheff SW Oxidative stress in the progression of Alzheimer disease in the frontal cortex. Curr Neuropharmacol — Toda N, Ayajiki K, Okamura T Cerebral blood flow regulation by nitric oxide in neurological disorders.

Can J Physiol Pharmacol — Casado Á, Encarnación López-Fernández M, Concepción Casado M, De La Torre R Lipid peroxidation and antioxidant enzyme activities in vascular and Alzheimer dementias. Spalletta G, Bernardini S, Bellincampi L, Federici G, Trequattrini A, Ciappi F, Bria P, Caltagirone C, Bossù P Glutathione S-transferase p1 and t1 gene polymorphisms predict longitudinal course and age at onset of Alzheimer disease.

Am J Geriatr Psychiatr — Am J Med Sci — Aoyama K, Nakaki T Impaired glutathione synthesis in neurodegeneration. Sultana R, Piroddi M, Galli F, Butterfield DA Protein levels and activity of some antioxidant enzymes in hippocampus of subjects with amnestic mild cognitive impairment.

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Swiss Medical Weekly Download references. Department of Toxicology, Chair of Toxicology, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, , Kraków, Poland.

Department of Neurology, Faculty of Medicine, Jagiellonian University, Medical College, Botaniczna 3, , Krakow, Poland. Laboratory of Drug Addiction Pharmacology, Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, , Kraków, Poland.

You can also search for this author in PubMed Google Scholar. Correspondence to Małgorzata Filip. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.

Reprints and permissions. Niedzielska, E. et al. Oxidative Stress in Neurodegenerative Diseases. Mol Neurobiol 53 , — Download citation. Received : 05 March Accepted : 01 July Published : 22 July Issue Date : August Anyone you share the following link with will be able to read this content:.

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Introduction Identifying factors that contribute to neurodegenerative processes in the brain is one of the major goals of modern medicine.

Full size image. Table 1 Enzymatic and non-enzymatic antioxidants against OS Full size table. Clinical Studies OS Biomarkers Post - mortem studies on tissue samples from SALS and FALS patients support the hypothesis of oxidative damage of proteins, lipids, and DNA.

Antioxidant Defense Biomarkers Most studies concerning antioxidant defense biomarkers in ALS patients have shown changes in peripheral tissues or in CSF but rarely in the brain. Pharmacological Strategies to Reduce OS Several pharmacotherapeutic agents with antioxidant properties have been attempted to slow ALS progression; however, most of them failed to do so Table 2.

Table 3 OS biomarkers in ALS animal model Full size table. Clinical Studies Oxidative Biomarkers Many studies have demonstrated the presence of OS and its markers in the brain and CSF in PD patients.

Anti-Parkinsonian Strategies to Restore Oxidative Balance Administration of zonisamide, an anticonvulsant drug prescribed to treat resting tremor in PD, inhibited the rise of 8-OHdG levels in the urine of PD patients.

Animal Studies Oxidative Biomarkers The most popular animal models of PD include pharmacological 6-hydroxydopamine 6-OHDA , 1-methylphenyl-1,2,3,6-tetrahydropyridine MPTP , rotenone, and paraquat as well as several genetic with mutations in the α-synuclein, PINK1, Parkin, or LRRK2 genes models [ ].

Table 5 Changes in OS and anti-OS defense biomarkers in toxin-based model of PD Full size table. Table 6 Therapeutic trials with substances possessing antioxidant properties in PD animal models and their influence on changes of biomarkers of OS and anti-oxidative defense Full size table.

Table 7 Therapeutic trials with anti-parkinsonian drugs in PD animal models and their influence on biomarkers of OS and of anti-oxidative defense Full size table.

Clinical Studies Oxidative Biomarkers The first report of the involvement of OS in AD pathology came from a paper by Martins et al. Antioxidant Defense Biomarkers Pivotal antioxidant enzymes, including GPx, CAT, and SOD, display changed levels in the brains of AD patients [ , ].

Pharmacological Strategy to Reduce OS As OS is present in AD patients, some clinical studies have aimed to test the ability of antioxidant substances to diminish ROS production and to alleviate or to slow the course of the disorder Table 8.

Table 9 Clinical trials of anti-Alzheimer drugs and their influence on OS biomarkers Full size table. Animal Studies Oxidative Biomarkers AD can be modeled by several procedures in animal.

Table 10 OS biomarkers and OS defense biomarkers in pharmacologically developed and in transgenic AD animal models Full size table. Table 12 Trials with anti-Alzheimer drugs in different AD animal models and their influence on oxidative damage and anti-oxidative defense biomarkers Full size table.

The consequences of these ion channel mutations related to oxidative stress are diverse and contribute to the pathogenesis of various diseases, such as neurological disorders, cardiac arrhythmias, and certain types of cancers.

Moreover, the aging process is linked with increased oxidative stress and a higher incidence of ion channel dysfunctions Uttara et al. Understanding the relationship between ion channel mutations and oxidative stress is essential for developing targeted therapeutic strategies.

Detailed information on specific potassium channel mutations and oxidative stress-related disorders, such as ataxias, can be found in these excellent manuscripts Figueroa et al.

This review will generally cover different ion channel mutations caused by oxidative stress in neurodegenerative diseases.

Neurodegenerative disorders affect millions of people worldwide. Brain atrophy is the hallmark of neurodegenerative diseases due to constant decline in neuronal function. Despite age being a significant risk factor for all neurodegenerative disorders, recent research indicates that genetic makeup and environmental factors greatly influence the risk as well Chen et al.

Although neurodegenerative disorders have distinct etiologies and develop in different brain sites, recent studies have observed that their effects on cellular and molecular mechanisms are similar Aborode et al. The central nervous system CNS has a significant oxidative potential because of its elevated oxygen usage.

However, the CNS is particularly vulnerable to oxidative stress because of the abundance of readily oxidizable substances, limited levels of primary and secondary antioxidants, elevated iron content in specific brain regions, the generation of ROS by various internal mechanisms, and the presence of non-replicating neurons Maher, ; Adibhatla and Hatcher, ; Guevara-García et al.

Figure 1 demonstrates the tendency of neurodegenerative diseases to progress as a result of oxidative stress Teleanu et al. Cells malfunction and even undergo apoptosis because the redox balance shifts to oxidative Lew et al.

Various neurodegenerative disorders are believed to be impacted by oxidative stress Figure 1. Furthermore, H 2 S at low concentrations lowers the level of ROS and thus protects neurons from oxidative stresses Shefa et al. It also protects neurons from apoptosis and degeneration Olas, Oxidative stress has been suggested as a factor in the development of various neurodegenerative disorders, including certain types of ataxias.

The etiology of the diseases is multifaceted, with genetic and familial investigations underscoring their heterogeneity Guevara-García et al.

Point mutations often lead to diminished expression of proteins specific to the mutated genes. The connection between neurodegenerative disorders and oxidative stress is dependent on molecular, in vitro , and animal studies findings. Nonetheless, conflicting results emerge from human biomarker studies, indicating the necessity for additional research on the role of redox in neurodegenerative disorders associated with channelopathies Li and Lester, ; Guevara-García et al.

Inherited Cerebellar Ataxias ICAs combine a group of complex and uncommon neurodegenerative conditions that impact the cerebellum, spinal cord, and peripheral nerves Coarelli et al. A person with ICA can experience balance, gait, speech, limb movement, eye movement, and cognitive difficulties.

A significant correlation exists between ataxia location and cerebellar neuropathology: hemisphere lesions result in limb or appendicular ataxia, while midline lesions result in gait ataxia Kashyap et al.

Spinocerebellar ataxia SCA is a subgroup of hereditary cerebellar ataxia, a progressive, neurodegenerative, heterogeneous, rare disease that affects the cerebellum Brooker et al.

The pathology of spinocerebellar ataxia is still unknown, but the principal cells involved in degeneration are Purkinje cells Koeppen, Purkinje cells regulate fine movement and muscle coordination.

Thus, a decline in the normal firing of the Purkinje cells leads to an excessive calcium influx and excitotoxicity Koeppen, ; Hosy et al. In the CNS, particularly the cerebellum, histopathology shows atrophy and enlargement of the lateral ventricles, loss of myelin in the frontal horn of the spinal cord, and axonal degeneration Bhandari et al.

There is an association between oxidative stress and several neurological disorders, including hereditary ataxias Guevara-García et al.

Numerous investigations have been conducted to prove the therapeutic roles of antioxidants in ICAs Sarva and Shanker, ; Braga Neto et al. Nevertheless, the results indicated that these antioxidants only partially alleviated symptoms of ICAs. This limitation may be because of the emphasis on clinical outcomes rather than a comprehensive understanding of the underlying molecular mechanisms associated with their approach to addressing oxidative stress Picher-Martel and Dupre, ; Lew et al.

The cause of ICAs is diverse Coarelli et al. The link between ataxia and oxidative stress depends mainly on molecular, in vitro , and in vivo studies. Recent findings, for example, have indicated that ataxin 2 and others are linked with the redox imbalance in this disease Guevara-García et al.

The significance of understanding the influence of oxidative stress on ion channels is crucial in considering ataxias. It is also needed to develop innovative approaches via alternative therapeutic intervention in ICA and related diseases.

A cerebellar cortex includes Purkinje cells that integrate all input into the cerebellum Hosy et al. A common feature of cerebellar ataxia is cerebellar atrophy and Purkinje neuron degeneration Koeppen, ; Cocozza et al. Purkinje neurons are unique in that they spike independently of synaptic stimulation.

SCA mouse models demonstrate that disruptions in the firing in Purkinje neurons considerably weaken motor function, indicating that this pacemaking ability of Purkinje neurons plays a critical role in motor coordination Kurian et al. In resting conditions, Purkinje neurons fire at an average frequency of 40 Hz with unvarying inter-spike interval duration.

Ion channels are predominantly responsible for maintaining this regularity Raman and Bean, ; Braga Neto et al. TABLE 3. Summary of some ion channels involved in oxidative stress-related neurodegenerative disorders.

Enzymatic antioxidants, such as superoxide dismutase, glutathione peroxidases, and catalase, along with non-enzymatic antioxidants like GSH and vitamins A, C, and E, counteract various types of oxidative stress Irato and Santovito, These antioxidants, whether endogenous or exogenous, reduce oxidative stress and scavenge ROS in ICAs, which could pave the way for a new ICA treatment Pandolfo, ; Lew et al.

Activating antioxidative transcription factor NRF2 could be a viable strategy to alleviate oxidative damage in ICAs Kavian et al. In response to oxidative stress, NRF2 modulates key antioxidant enzymes, which, either directly or indirectly, regulate redox homeostasis Liu et al.

Compared to agents possessing only one of these actions, AM inhibited toxicity and apoptosis mediated by the generation of ROS Callaway et al. Therefore, it is important to understand the link between the strategy targeting specific ion channels and antioxidants in mediating the progression of ICAs.

The dopamine secretion by these neurons is crucial for controlling movement ease and balance. The etiologies of PD are still questionable. Leucine-rich repeat kinase 2 LRRK2 Mutations are one of the causative genetic variants that account for several autosomal, dominantly inherited PD Blauwendraat et al.

It has also been discovered that other genes, including ATP13A2, SNCA, PINK, GIGYF2, HTRA2, and DJ1, can cause familiar and early-onset PD. Among their functions are the degradation of ubiquitin proteins, the response to oxidative stress, apoptosis, cell survival, and mitochondrial function Maiti et al.

Oxidative stress significantly promotes the erosion of dopaminergic neurons in PD Dias et al. Oxygen is essential for brain function, and a large amount of oxygen is converted into ROS. Oxidative stress is closely related to other components of the degenerative process, like excitotoxicity, nitric oxide toxicity, and mitochondrial dysfunction Jenner, ; Henchcliffe and Beal, Several genes associated with familial PD, including parkin, alpha-synuclein, LRRK2, DJ-1, and PINK-1, have been identified, providing important understandings of the molecular pathways underlying the disease pathogenesis, as well as highlighting earlier mysterious mechanisms where oxidative stress plays a role in the disease Dias et al.

As oxidative stress leads to programmed cell death, the mitochondrial condition of GSH has gained recognition as a significant indicator of this occurrence Chang and Chen, Targeting ion channels provides an intriguing mechanistic strategy to address the progression of PD and other neurodegenerative disorders because of their important roles in neuronal activities Braga Neto et al.

As a result, there have been numerous efforts to address these pathways in order to provide neuroprotection Daniel et al. While several of these drugs in preclinical studies have demonstrated positive outcomes, none of these interventions have effectively transitioned into clinical application Jenner, In the field of ion channel drug discovery, a significant challenge is preventing side effects arising from both target and off-target mechanisms.

Additionally, subtype selectivity is challenging when various homologous members belong to the same subfamily Brown et al. Ion channel malfunction is a common factor in neurological disorders, even when various genes are implicated as the root causes of these diseases.

The malfunction of ion channels can result from changes in the intracellular redox environment, which alter how these channels function. Despite recent advancements, the precise mechanisms of reactive oxygen species ROS -mediated neurodegenerative diseases remain partially understood.

The role of ion channels in neurodegenerative disorders associated with oxidative stress has now been recognized, as they experience functional adjustments in such conditions.

However, the significance of targeting ion channels therapeutically varies depending on the disease and the tissues in which these channels are active. Ultimately, neurodegenerative diseases may be effectively treated with a combination of ion channel-modulating therapy and antioxidant medication.

More research on the function of ion channels in oxidative stress may provide a platform for exploring new therapeutic approaches for treating many neurodegenerative diseases associated with oxidative stress. RO: Visualization, Writing—original draft.

AA: Writing—review and editing. RSO: Visualization, Writing—original draft. LL: Writing—review and editing. NC: Writing—review and editing. AMA: Writing—review and editing. Y-WN: Supervision, Writing—review and editing. MZ: Conceptualization, Supervision, Writing—review and editing.

The study was supported by a 23AIREA grant from the American Heart Association and a 4R33NS grant from NIH awarded to MZ. We thank King Fahad Medical City Writing Center for revising the manuscript. Thanks to Rahaf and Raghad Alabdulsalam for their technical Support.

The figures were created with BioRender and published with permission. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

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Numerous neurodegenerative diseases result from altered ion Herbal weight loss aids function and mutations. The intracellular redox status can neurodebenerative alter the gating characteristics Oxidativr ion Oxidative stress and neurodegenerative diseases. Neufodegenerative oxygen and nitrogen species strsss trigger posttranslational alterations Sports nutrition guidelines target znd sites within the subunits responsible for channel assembly. These alterations Healthy fats for endurance athletes Oxidative stress and neurodegenerative diseases adjustment of neurpdegenerative residues through redox reactions induced by reactive oxygen species ROSnitration, and S-nitrosylation assisted by nitric oxide of tyrosine residues through peroxynitrite. Several ion channels have been directly investigated for their functional responses to oxidizing agents and oxidative stress. The potential correlation between oxidative stress and ion channels could hold promise for developing innovative therapies for common neurodegenerative diseases. Reactive oxygen species ROS are generated by living organisms as a result of their regular cellular metabolic processes and environmental factors, such as smoking, air pollutants, UV radiation, alcohol consumption, infections, non-steroidal anti-inflammatory drugs NSAIDsand inflammation Valko et al. Editor-in-Chief: Ferdinando Nicoletti Department Sports nutrition guidelines Pharmaceutical Sciences Biomass energy conversion Rome'da Sapienza' Rome Oxidative stress and neurodegenerative diseases. ISSN Print : X Neurodegeherative Online : DOI: neurodegenedative Free radicals are common outcome of siseases aerobic cellular metabolism. In-built antioxidant system of body plays its decisive role in prevention of any loss due to free radicals. However, imbalanced defense mechanism of antioxidants, overproduction or incorporation of free radicals from environment to living system leads to serious penalty leading to neuro-degeneration. Neural cells suffer functional or sensory loss in neurodegenerative diseases.


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