ArticleNeurochemical research2013
Effect of α-synuclein on amyloid β-induced toxicity: relevance to Lewy body variant of Alzheimer disease.
Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 35 citations in OpenAlex.
- Targeting protein aggregate co-pathologies in neurodegeneration: a viable therapeutic strategy?Molecular neurodegeneration advances · 2026Review
- Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein.Molecular neurodegeneration · 2025Review
- Effect of Aflatoxin B1 on the Nervous System: A Systematic Review and Network Analysis Highlighting Alzheimer's Disease.Biology · 2025Review
- Cerebrospinal fluid biomarkers profile in scans without evidence of dopaminergic deficits (SWEDD).IBRO neuroscience reports · 2023Article
- Potential value of cerebrospinal fluid α-synuclein in the identification of postoperative delirium undergoing knee/hip arthroplasty: The perioperative neurocognitive disorder and biomarker lifestyle study.Frontiers in neuroscience · 2022Article
- Curcumin slows the progression of Alzheimer's disease by modulating mitochondrial stress responses via JMJD3-H3K27me3-BDNF axis.American journal of translational research · 2021Article
- Cerebrospinal fluid α-synuclein predicts neurodegeneration and clinical progression in non-demented elders.Translational neurodegeneration · 2020Article
- Cause and consequence of Aβ - Lipid interactions in Alzheimer disease pathogenesis.Biochimica et biophysica acta. Biomembranes · 2018Review
- Insights into the Molecular Mechanisms of Alzheimer's and Parkinson's Diseases with Molecular Simulations: Understanding the Roles of Artificial and Pathological Missense Mutations in Intrinsically Disordered Proteins Related to Pathology.International journal of molecular sciences · 2018Review
- Amyloid β-peptides 1-40 and 1-42 form oligomers with mixed β-sheets.Chemical science · 2017Article
- Activation of Mitochondrial Complex II-Dependent Respiration Is Beneficial for α-Synucleinopathies.Molecular neurobiology · 2016Article
- Neuropsychiatric Disturbances in Alzheimer's Disease: What Have We Learned from Neuropathological Studies?Current Alzheimer research · 2016Review
- Cerebrospinal Fluid Aβ42 Levels: When Physiological Become Pathological State.CNS neuroscience & therapeutics · 2015Review
- Amyloid β oligomers in Alzheimer's disease pathogenesis, treatment, and diagnosis.Acta neuropathologica · 2015Review
- Mini review: linkage between α-Synuclein protein and cognition.Translational neurodegeneration · 2015Article
- Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease.Acta neuropathologica communications · 2014Review
- New α- and γ-synuclein immunopathological lesions in human brain.Acta neuropathologica communications · 2014Article
- Cross dimerization of amyloid-β and αsynuclein proteins in aqueous environment: a molecular dynamics simulations study.PloS one · 2014Article
- Genetic Association between Presenilin 2 Polymorphisms and Alzheimer's Disease and Dementia of Lewy Body Type in a Japanese Population.Dementia and geriatric cognitive disorders extraArticle
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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
Alzheimer's disease, the most prevalent age-related neurodegenerative disease, is characterized by the presence of extracellular senile plaques composed of amyloid-beta (Aβ) peptide and intracellular neurofibrillary tangles. More than 50 % of Alzheimer's disease (AD) patients also exhibit abundant accumulation of α-synuclein (α-Syn)-positive Lewy bodies. This Lewy body variant of AD (LBV-AD) is associated with accelerated cognitive dysfunction and progresses more rapidly than pure AD. In addition, it has been suggested that Aβ and α-Syn can directly interact. In this study we investigated the effect of α-Syn on Aβ-induced toxicity in cortical neurons. In order to mimic the intracellular accumulation of α-Syn observed in the brain of LBV-AD patients, we used valproic acid (VPA) to increase its endogenous expression levels. The release of α-Syn from damaged presynaptic terminals that occurs during the course of the disease was simulated by challenging cells with recombinant α-Syn. Our results showed that either VPA-induced α-Syn upregulation or addition of recombinant α-Syn protect primary cortical neurons from soluble Aβ1-42 decreasing the caspase-3-mediated cell death. It was also found that neuroprotection against Aβ-induced toxicity mediated by α-Syn overexpression involves the PI3K/Akt cell survival pathway. Furthermore, recombinant α-Syn was shown to directly interact with Aβ1-42 and to decrease the levels of Aβ1-42 oligomers, which might explain its neuroprotective effect. In conclusion, we demonstrate that either endogenous or exogenous α-Syn can be neuroprotective against Aβ-induced cell death, suggesting a cell defence mechanism during the initial stages of the mixed pathology.
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