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  Reduced oxidative damage in ALS by high-dose enteral melatonin treatment

Weishaupt, J. H., Bartels, C., Pölking, E., Dietrich, J., Rohde, G., Poeggeler, B., et al. (2006). Reduced oxidative damage in ALS by high-dose enteral melatonin treatment. Journal of Pineal Research, 41(4), 313-323. doi:10.1111/j.1600-079X.2006.00377.x.

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 Urheber:
Weishaupt, Jochen H., Autor
Bartels, Claudia1, Autor           
Pölking, Esther, Autor
Dietrich, Jeannine1, Autor           
Rohde, Gundula, Autor
Poeggeler, Burkhard, Autor
Mertens, Nina1, Autor           
Sperling, Swetlana1, Autor           
Bohn, Matthias, Autor
Hüther, Gerald, Autor
Schneider, Armin, Autor
Bach, Alfred, Autor
Sirén, Anna-Leena1, Autor           
Hardeland, Rüdiger, Autor
Bähr, Mathias, Autor
Nave, Klaus-Armin2, Autor           
Ehrenreich, Hannelore1, Autor           
Affiliations:
1Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173651              
2Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173664              

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Schlagwörter: amyotrophic lateral sclerosis; human safety study; melatonin; motoneurons; neuroprotection; reactive oxygen species; transgenic models AMYOTROPHIC-LATERAL-SCLEROSIS; GLUTAMATE TRANSPORTER EAAT2; MOTOR-NEURON DEGENERATION; TRANSGENIC MOUSE MODEL; SUPEROXIDE-DISMUTASE; VITAMIN-E; PROLONGS SURVIVAL; MODIFIED PROTEINS; NERVOUS-SYSTEM; CLINICAL-TRIAL
 Zusammenfassung: Amyotrophic lateral sclerosis (ALS) is the collective term for a fatal motoneuron disease of different etiologies, with oxidative stress as a common molecular denominator of disease progression. Melatonin is an amphiphilic molecule with a unique spectrum of antioxidative effects not conveyed by classical antioxidants. In preparation of a possible future clinical trial, we explored the potential of melatonin as neuroprotective compound and antioxidant in: (1) cultured motoneuronal cells (NSC-34), (2) a genetic mouse model of ALS (SOD1(G93A)-transgenic mice), and (3) a group of 31 patients with sporadic ALS. We found that melatonin attenuates glutamate-induced cell death of cultured motoneurons. In SOD1(G93A)-transgenic mice, high-dose oral melatonin delayed disease progression and extended survival. In a clinical safety study, chronic high-dose (300 mg/day) rectal melatonin was well tolerated during an observation period of up to 2 yr. Importantly, circulating serum protein carbonyls, which provide a surrogate marker for oxidative stress, were elevated in ALS patients, but were normalized to control values by melatonin treatment. This combination of preclinical effectiveness and proven safety in humans suggests that high-dose melatonin is suitable for clinical trials aimed at neuroprotection through antioxidation in ALS.

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Sprache(n): eng - English
 Datum: 2006-11
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1111/j.1600-079X.2006.00377.x
 Art des Abschluß: -

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Titel: Journal of Pineal Research
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: Copenhagen, DK : Munksgaard International Publishers
Seiten: - Band / Heft: 41 (4) Artikelnummer: - Start- / Endseite: 313 - 323 Identifikator: ISSN: 0742-3098
CoNE: https://pure.mpg.de/cone/journals/resource/954925540178