Search results for "BMAA"

Hypothesis: Etiologic and Molecular Mechanistic Leads for Sporadic Neurodegenerative Diseases Based on Experience With Western Pacific ALS/PDC

2019

Seventy years of research on Western Pacific amyotrophic lateral sclerosis and Parkinsonism-dementia Complex (ALS/PDC) have provided invaluable data on the etiology, molecular pathogenesis and latency of this disappearing, largely environmental neurodegenerative disease. ALS/PDC is linked to genotoxic chemicals (notably methylazoxymethanol, MAM) derived from seed of the cycad plant (Cycas spp.) that were used as a traditional food and/or medicine in all three disease-affected Western Pacific populations. MAM, nitrosamines and hydrazines generate methyl free radicals that damage DNA (in the form of O6-methylguanine lesions) that can induce mutations in cycling cells and degenerative changes …

Separazione della beta-N-metilammino-L-alanina (BMAA) in campioni di liquor cefalorachidiano mediante HPLC con rilevazione fluorimetrica

2011

TOXICITY OF B-N-OXALYLAMINO-L-ALANINE ANDB-N-METHYLAMINO-L-ALANINE IN NIH3T3 CELLS IS MEDIATED BY INHIBITIONOF THE XC¯ ANTIPORTER

2012

Beta-N-oxalylamino-L-alanine (BOAA) and beta-N-methylamino-L-alanine (BMAA) are two non-protein amino acids reported to induce neuronal degeneration. They have been involved in the pathogenesis of rare motor neuron diseases, as neurolathyrism or the ALS-Parkinson-Dementia complex of Guam. The mechanisms by which BOAA and BMAA toxicity is explicated is still unknown, but there is evidence that it might involve the inhibition of Xc¯ antiporter, that is the rate-limiting transporter of the synthesis of intracellular glutathione. In the present study, we investigated the mechanisms of BOAA and BMAA toxicity in the non-neuronal NIH3T3 cells. First, we treated NIH3T3 cells with BOAA or BMAA at di…