ArticleScientific reports2015
Environmental neurotoxin interaction with proteins: Dose-dependent increase of free and protein-associated BMAA (β-N-methylamino-L-alanine) in neonatal rat brain.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Evidence that non-cognate proteinogenic amino acids generate immunogenic neoepitopes.The Journal of biological chemistry · 2026Review
- Review
- The herbicides glyphosate and glufosinate and the cyanotoxin β-N-methylamino-l-alanine induce long-term motor disorders following postnatal exposure: the importance of prior asymptomatic maternal inflammatory sensitization.Frontiers in neuroscience · 2023Article
- Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases? A Response to a Critical Review of the BMAA Hypothesis.Neurotoxicity research · 2021Article
- The cyanobacterial neurotoxin β-N-methylamino-L-alanine (BMAA) targets the olfactory bulb region.Archives of toxicology · 2020Article
- Mitotically heritable effects of BMAA on striatal neural stem cell proliferation and differentiation.Cell death & disease · 2019Article
- Dose-Dependent Adult Neurodegeneration in a Rat Model After Neonatal Exposure to β-N-Methylamino-L-Alanine.Neurotoxicity research · 2019Article
- Assessing Environmental Exposure to β-N-Methylamino-L-Alanine (BMAA) in Complex Sample Matrices: a Comparison of the Three Most Popular LC-MS/MS Methods.Neurotoxicity research · 2018Article
- Perinatal Exposure to the Cyanotoxin β-N-Méthylamino-L-Alanine (BMAA) Results in Long-Lasting Behavioral Changes in Offspring-Potential Involvement of DNA Damage and Oxidative Stress.Neurotoxicity research · 2018Article
- Review
- Melatonin Promotes Brain-Derived Neurotrophic Factor (BDNF) Expression and Anti-Apoptotic Effects in Neonatal Hemolytic Hyperbilirubinemia via a Phospholipase (PLC)-Mediated Mechanism.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- MALDI imaging delineates hippocampal glycosphingolipid changes associated with neurotoxin induced proteopathy following neonatal BMAA exposure.Biochimica et biophysica acta. Proteins and proteomics · 2017Article
- Imaging mass spectrometry in drug development and toxicology.Archives of toxicology · 2017Review
- β-N-Methylamino-L-alanine (BMAA) perturbs alanine, aspartate and glutamate metabolism pathways in human neuroblastoma cells as determined by metabolic profiling.Amino acids · 2017Article
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Methylamino-L-alanine (BMAA) is implicated in the aetiology of neurodegenerative disorders. Neonatal exposure to BMAA induces cognitive impairments and progressive neurodegenerative changes including intracellular fibril formation in the hippocampus of adult rats. It is unclear why the neonatal hippocampus is especially vulnerable and the critical cellular perturbations preceding BMAA-induced toxicity remains to be elucidated. The aim of this study was to compare the level of free and protein-associated BMAA in neonatal rat brain and peripheral tissues after different exposures to BMAA. Ultra-high performance liquid chromatography-tandem mass spectrometry analysis revealed that BMAA passed the neonatal blood-brain barrier and was distributed to all studied brain areas. BMAA was also associated to proteins in the brain, especially in the hippocampus. The level in the brain was, however, considerably lower compared to the liver that is not a target organ for BMAA. In contrast to the liver there was a significantly increased level of protein-association of BMAA in the hippocampus and other brain areas following repeated administration suggesting that the degradation of BMAA-associated proteins may be lower in neonatal brain than in the liver. Additional evidence is needed in support of a role for protein misincorporation in the neonatal hippocampus for long-term effects of BMAA.
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