ArticlePloS one2013
Impairment of mitochondria in adult mouse brain overexpressing predominantly full-length, N-terminally acetylated human α-synuclein.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Amyloid accelerator polyphosphate fits as the mystery density in α-synuclein fibrils.PLoS biology · 2024Article
- Glutathione Depletion and Concomitant Elevation of Susceptibility in Patients with Parkinson's Disease: State-of-the-Art MR Spectroscopy and Neuropsychological Study.ACS chemical neuroscience · 2023Article
- Characterization of Molecular Tweezer Binding on α-Synuclein with Native Top-Down Mass Spectrometry and Ion Mobility-Mass Spectrometry Reveals a Mechanism for Aggregation Inhibition.Journal of the American Society for Mass Spectrometry · 2023Article
- Oleuropein confers neuroprotection against rotenone-induced model of Parkinson's disease via BDNF/CREB/Akt pathway.Scientific reports · 2023Article
- Post-translational modification and mitochondrial function in Parkinson's disease.Frontiers in molecular neuroscience · 2023Review
- Genes Implicated in Familial Parkinson's Disease Provide a Dual Picture of Nigral Dopaminergic Neurodegeneration with Mitochondria Taking Center Stage.International journal of molecular sciences · 2021Review
- Misfolded α-synuclein causes hyperactive respiration without functional deficit in live neuroblastoma cells.Disease models & mechanisms · 2020Article
- Alpha-synuclein-induced mitochondrial dysfunction is mediated via a sirtuin 3-dependent pathway.Molecular neurodegeneration · 2020Article
- Current Evidence for a Bidirectional Loop Between the Lysosome and Alpha-Synuclein Proteoforms.Frontiers in cell and developmental biology · 2020Review
- LRRK2 and α-Synuclein: Distinct or Synergistic Players in Parkinson's Disease?Frontiers in neuroscience · 2020Review
- Enhanced mitochondrial inhibition by 3,4-dihydroxyphenyl-acetaldehyde (DOPAL)-oligomerized α-synuclein.Journal of neuroscience research · 2019Article
- The role of lipids in α-synuclein misfolding and neurotoxicity.The Journal of biological chemistry · 2019Review
- The unlikely partnership between LRRK2 and α-synuclein in Parkinson's disease.The European journal of neuroscience · 2019Review
- The genetic architecture of mitochondrial dysfunction in Parkinson's disease.Cell and tissue research · 2018Review
- Spatially-Resolved Top-down Proteomics Bridged to MALDI MS Imaging Reveals the Molecular Physiome of Brain Regions.Molecular & cellular proteomics : MCP · 2018Article
- Stimulation of synaptoneurosome glutamate release by monomeric and fibrillated α-synuclein.Journal of neuroscience research · 2017Article
- The Role of Autophagy, Mitophagy and Lysosomal Functions in Modulating Bioenergetics and Survival in the Context of Redox and Proteotoxic Damage: Implications for Neurodegenerative Diseases.Aging and disease · 2016Review
- Intracellular repair of oxidation-damaged α-synuclein fails to target C-terminal modification sites.Nature communications · 2016Article
- Article
- Seeking a mechanism for the toxicity of oligomeric α-synuclein.Biomolecules · 2015Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
While most forms of Parkinson's Disease (PD) are sporadic in nature, a small percentage of PD have genetic causes as first described for dominant, single base pair changes as well as duplication and triplication in the α-synuclein gene. The α-synuclein gene encodes a 140 amino acid residue protein that interacts with a variety of organelles including synaptic vesicles, lysosomes, endoplasmic reticulum/Golgi vesicles and, reported more recently, mitochondria. Here we examined the structural and functional interactions of human α-synuclein with brain mitochondria obtained from an early, pre-manifest mouse model for PD over-expressing human α-synuclein (ASOTg). The membrane potential in ASOTg brain mitochondria was decreased relative to wildtype (WT) mitochondria, while reactive oxygen species (ROS) were elevated in ASOTg brain mitochondria. No selective interaction of human α-synuclein with mitochondrial electron transport complexes cI-cV was detected. Monomeric human α-synuclein plus carboxyl terminally truncated forms were the predominant isoforms detected in ASOTg brain mitochondria by 2-dimensional PAGE (Native/SDS) and immunoblotting. Oligomers or fibrils were not detected with amyloid conformational antibodies. Mass spectrometry of human α-synuclein in both ASOTg brain mitochondria and homogenates from surgically resected human cortex demonstrated that the protein was full-length and postranslationally modified by N-terminal acetylation. Overall the study showed that accumulation of full-length, N-terminally acetylated human α-synuclein was sufficient to disrupt brain mitochondrial function in adult mice.
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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.