ArticleProteomics2017
Exposure to BMAA mirrors molecular processes linked to neurodegenerative disease.
Article in Proteomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- Alcohol exposure alters the diversity and composition of oral microbiome.Frontiers in cellular and infection microbiology · 2025Article
- Selection, characterization, and biosensing applications of DNA aptamers targeting cyanotoxin BMAA.RSC advances · 2024Article
- Gut Symptoms, Gut Dysbiosis and Gut-Derived Toxins in ALS.International journal of molecular sciences · 2024Review
- Evaluation of cyanotoxin L-BMAA effect on α-synuclein and TDP43 proteinopathy.Frontiers in immunology · 2024Article
- Chronic BMAA exposure combined with TDP-43 mutation elicits motor neuron dysfunction phenotypes in mice.Neurobiology of aging · 2023Article
- Non-Proteinogenic Amino Acid β-N-Methylamino-L-Alanine (BMAA): Bioactivity and Ecological Significance.Toxins · 2022Review
- The Cyanotoxin 2,4-DAB Reduces Viability and Causes Behavioral and Molecular Dysfunctions Associated with Neurodegeneration in Larval Zebrafish.Neurotoxicity research · 2022Article
- Marine Neurotoxins' Effects on Environmental and Human Health: An OMICS Overview.Marine drugs · 2021Review
- β-Methylamino-L-alanine-induced protein aggregation in vitro and protection by L-serine.Amino acids · 2021Article
- Cyanobacteria, Cyanotoxins, and Neurodegenerative Diseases:International journal of molecular sciences · 2021Review
- Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases? A Response to a Critical Review of the BMAA Hypothesis.Neurotoxicity research · 2021Article
- BMAA and MCLR Interact to Modulate Behavior and Exacerbate Molecular Changes Related to Neurodegeneration in Larval Zebrafish.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Misincorporation Proteomics Technologies: A Review.Proteomes · 2021Review
- l-Serine Reduces Spinal Cord Pathology in a Vervet Model of Preclinical ALS/MND.Journal of neuropathology and experimental neurology · 2020Article
- The mechanism of β-The Journal of biological chemistry · 2020Article
- Microbial BMAA and the Pathway for Parkinson's Disease Neurodegeneration.Frontiers in aging neuroscience · 2020Article
- The Cyanotoxin and Non-protein Amino Acid β-Methylamino-L-Alanine (L-BMAA) in the Food Chain: Incorporation into Proteins and Its Impact on Human Health.Neurotoxicity research · 2019Review
- Review
- Dietary and Environmental Risk Factors in Parkinson's and Alzheimer's Disease: A Semi-Quantitative Pilot Study.Annals of Indian Academy of NeurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The goal of this study is to investigate the molecular pathways perturbed by in vitro exposure of beta-methylamino-L-alanine (BMAA) to NSC-34 cells via contemporary proteomics. Our analysis of differentially regulated proteins reveals significant enrichment (p < 0.01) of pathways related to ER stress, protein ubiquitination, the unfolded protein response, and mitochondrial dysfunction. Upstream regulator analysis indicates that exposure to BMAA induces activation of transcription factors (X-box binding protein 1; nuclear factor 2 erythroid like 2; promyelocytic leukemia) involved in regulation of the UPR, oxidative stress, and cellular senescence. Furthermore, the authors examine the hypothesis that BMAA causes protein damage via misincorporation in place of L-Serine. The authors are unable to detect misincorporation of BMAA into protein via analysis of cellular protein, secreted protein, targeted detection of BMAA after protein hydrolysis, or through the use of in vitro protein translation kits.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.