ArticleActa neuropathologica2015
Aβ43 is neurotoxic and primes aggregation of Aβ40 in vivo.
Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 45 citations in OpenAlex.
- Aging brain lesions of a 60-year-old Bornean orangutan (Pongo pygmaeus).The Journal of veterinary medical science · 2026Article
- Amyloid-beta induces distinct forms of cell death in different neuronal populations.Cell death and differentiation · 2026Article
- Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026Review
- Exploring Autophagy Inducing Molecules: Targeting Diverse Pathways in Alzheimer's Disease Management.Medicinal research reviews · 2026Review
- The molecular spectrum of amyloid-beta (Aβ) in neurodegenerative diseases beyond Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2024Article
- Senile plaques and phosphorylated tau deposition in a super-aged rhesus monkey (Macaca mulatta).The Journal of veterinary medical science · 2023Article
- Different Aβ43 deposition patterns in the brains of aged dogs, sea lions, and cats.The Journal of veterinary medical science · 2022Article
- Exploring Aβ Proteotoxicity and Therapeutic Candidates UsingInternational journal of molecular sciences · 2021Review
- Critical Appraisal of Amyloid Lowering Agents in AD.Current neurology and neuroscience reports · 2021Review
- Aβ43 aggregates exhibit enhanced prion-like seeding activity in mice.Acta neuropathologica communications · 2021Article
- Alternative Targets to Fight Alzheimer's Disease: Focus on Astrocytes.Biomolecules · 2021Review
- PICALM rescues glutamatergic neurotransmission, behavioural function and survival in a Drosophila model of Aβ42 toxicity.Human molecular genetics · 2020Article
- Reduced Influence of apoE on Aβ43 Aggregation and Reduced Vascular Aβ43 Toxicity as Compared with Aβ40 and Aβ42.Molecular neurobiology · 2020Article
- Decreased Deposition of Beta-Amyloid 1-38 and Increased Deposition of Beta-Amyloid 1-42 in Brain Tissue of Presenilin-1 E280A Familial Alzheimer's Disease Patients.Frontiers in aging neuroscience · 2020Article
- Aβ43 in human Alzheimer's disease: effects of active Aβ42 immunization.Acta neuropathologica communications · 2019Article
- Role of Amyloid Precursor Protein (APP) and Its Derivatives in the Biology and Cell Fate Specification of Neural Stem Cells.Molecular neurobiology · 2018Review
- Amyloid assembly and disassembly.Journal of cell science · 2018Review
- Short Aβ peptides attenuate Aβ42 toxicity in vivo.The Journal of experimental medicine · 2018Article
- UsingBioMed research international · 2018Review
- Induction of Amyloid-β42 Production by Fipronil and Other Pyrazole Insecticides.Journal of Alzheimer's disease : JAD · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The involvement of Amyloid-β (Aβ) in the pathogenesis of Alzheimer's disease (AD) is well established. However, it is becoming clear that the amyloid load in AD brains consists of a heterogeneous mixture of Aβ peptides, implying that a thorough understanding of their respective role and toxicity is crucial for the development of efficient treatments. Besides the well-studied Aβ40 and Aβ42 species, recent data have raised the possibility that Aβ43 peptides might be instrumental in AD pathogenesis, because they are frequently observed in both dense and diffuse amyloid plaques from human AD brains and are highly amyloidogenic in vitro. However, whether Aβ43 is toxic in vivo is currently unclear. Using Drosophila transgenic models of amyloid pathology, we show that Aβ43 peptides are mainly insoluble and highly toxic in vivo, leading to the progressive loss of photoreceptor neurons, altered locomotion and decreased lifespan when expressed in the adult fly nervous system. In addition, we demonstrate that Aβ43 species are able to trigger the aggregation of the typically soluble and non-toxic Aβ40, leading to synergistic toxic effects on fly lifespan and climbing ability, further suggesting that Aβ43 peptides could act as a nucleating factor in AD brains. Altogether, our study demonstrates high pathogenicity of Aβ43 species in vivo and supports the idea that Aβ43 contributes to the pathological events leading to neurodegeneration in AD.
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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.