β-N-methylamino-L-alanine Enhances Neurotoxicity Through Multiple Mechanisms

Authors

Doug Lobner, Marquette UniversityFollow
Peachy Mae T. Piana, Marquette University
Abed K. Salous, Marquette University
Robert W. Peoples, Marquette UniversityFollow

Document Type

Article

Language

eng

Format of Original

7 p.

Publication Date

2-2007

Publisher

Elsevier

Source Publication

Neurobiology of Disease

Source ISSN

0969-9961

Original Item ID

doi: 10.1016/j.nbd.2006.10.002

Abstract

The idea that the environmental toxin β-N-methylamino-l-alanine (BMAA) is involved in neurodegenerative diseases on Guam has risen and fallen over the years. The theory has gained greater interest with recent reports that BMAA is biomagnified, is widely distributed around the planet, and is present in the brains of Alzheimer's patients in Canada. We provide two important new findings. First, we show that BMAA at concentrations as low as 10 μM can potentiate neuronal injury induced by other insults. This is the first evidence that BMAA at concentrations below the mM range can enhance death of cortical neurons and illustrates potential synergistic effects of environmental toxins with underlying neurological conditions. Second, we show that the mechanism of BMAA toxicity is threefold: it is an agonist for NMDA and mGluR5 receptors, and induces oxidative stress. The results provide further support for the hypothesis that BMAA plays a role in neurodegenerative diseases.

Comments

Accepted version. Neurobiology of Disease, Vol. 25, No. 2 (February 2007): 360-366. DOI. © 2007 Elsevier. Used with permission.

Recommended Citation

Lobner, Doug; Piana, Peachy Mae T.; Salous, Abed K.; and Peoples, Robert W., "β-N-methylamino-L-alanine Enhances Neurotoxicity Through Multiple Mechanisms" (2007). Biomedical Sciences Faculty Research and Publications. 102.
https://epublications.marquette.edu/biomedsci_fac/102