β-Lactam antibiotics offer neuroprotection by increasing glutamate transporter expression

Jeffrey D. Rothstein (), Sarjubhai Patel, Melissa R. Regan, Christine Haenggeli, Yanhua H. Huang, Dwight E. Bergles, Lin Jin, Margaret Dykes Hoberg, Svetlana Vidensky, Dorothy S. Chung, Shuy Vang Toan, Lucie I. Bruijn, Zao-zhong Su, Pankaj Gupta and Paul B. Fisher
Additional contact information
Jeffrey D. Rothstein: Department of Neurology
Sarjubhai Patel: Department of Neurology
Melissa R. Regan: Department of Neurology
Christine Haenggeli: Department of Neurology
Yanhua H. Huang: Johns Hopkins University
Dwight E. Bergles: Johns Hopkins University
Lin Jin: Department of Neurology
Margaret Dykes Hoberg: Department of Neurology
Svetlana Vidensky: Department of Neurology
Dorothy S. Chung: Department of Neurology
Shuy Vang Toan: Department of Neurology
Lucie I. Bruijn: The ALS Association
Zao-zhong Su: Columbia University Medical Center, College of Physicians and Surgeons
Pankaj Gupta: Columbia University Medical Center, College of Physicians and Surgeons
Paul B. Fisher: Columbia University Medical Center, College of Physicians and Surgeons

Nature, 2005, vol. 433, issue 7021, 73-77

Abstract: Rewrite the pharmacopoeia The β-lactam antibiotics — penicillin and its semisynthetic derivatives — act by inhibiting bacterial synthetic pathways, and their success has in part been because they have little effect on their hosts. So it's a complete surprise to find that many of these β-lactams also act on the dominant excitatory neurotransmitter transporter system in the mammalian central nervous system. The mechanism of action involves activation of GLT1, the gene for glutamate transport. In animal models of ischaemic injury and motor neuron degeneration, ceftriaxone is neuroprotective, and in the animal model of the fatal disease amyotrophic lateral sclerosis (Lou Gehrig's disease), it increases the survival rate of mice. These studies provide a completely new drug target for scores of highly safe pharmaceuticals and may lead to new therapies for neurological disease.

Date: 2005
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DOI: 10.1038/nature03180

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