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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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 Creators:
Weishaupt, Jochen H., Author
Bartels, Claudia1, Author           
Pölking, Esther, Author
Dietrich, Jeannine1, Author           
Rohde, Gundula, Author
Poeggeler, Burkhard, Author
Mertens, Nina1, Author           
Sperling, Swetlana1, Author           
Bohn, Matthias, Author
Hüther, Gerald, Author
Schneider, Armin, Author
Bach, Alfred, Author
Sirén, Anna-Leena1, Author           
Hardeland, Rüdiger, Author
Bähr, Mathias, Author
Nave, Klaus-Armin2, Author           
Ehrenreich, Hannelore1, Author           
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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Free keywords: 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
 Abstract: 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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Language(s): eng - English
 Dates: 2006-11
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 292143
ISI: 000240921200003
ISI: 000240921200003
DOI: 10.1111/j.1600-079X.2006.00377.x
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Title: Journal of Pineal Research
  Alternative Title : J Pineal Res
Source Genre: Journal
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Pages: - Volume / Issue: 41 (4) Sequence Number: - Start / End Page: 313 - 323 Identifier: ISSN: 0742-3098