Gliotoxicity of the cyanotoxin, β-methyl-amino-L-alanine (BMAA)

Alexander S. Chiu, Michelle M. Gehringer, Nady Braidy, Gilles J. Guillemin, Jeffrey H. Welch, Brett A. Neilan*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

42 Citations (Scopus)

Abstract

The amino acid variant β-methyl-amino-L-alanine (BMAA) has long been associated with the increased incidence and progression of the amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC). Previous studies have indicated that BMAA damages neurons via excitotoxic mechanisms. We have challenged rat olfactory ensheathing cells (OECs) with exogenous BMAA and found it to be cytotoxic. BMAA also induces a significant increase in Ca2+ influx, enhanced production of reactive oxygen species (ROS), and disrupts mitochondrial activity in OECs. This is the first study investigating BMAA toxicity using pure glial cells. These findings align BMAA with the three proposed mechanisms of degeneration in ALS, those being non-cell autonomous death, excitotoxicity and mitochondrial dysfunction.

Original languageEnglish
Article number1482
Pages (from-to)1-5
Number of pages5
JournalScientific Reports
Volume3
DOIs
Publication statusPublished - 2013
Externally publishedYes

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