ArticleeLife2020
Application of optogenetic Amyloid-β distinguishes between metabolic and physical damages in neurodegeneration.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 43 citations in OpenAlex.
- Review
- Optogenetics to biomolecular phase separation in neurodegenerative diseases.Molecules and cells · 2025Review
- Article
- Modeling Alzheimer's Disease: A Review of Gene-Modified and Induced Animal Models, Complex Cell Culture Models, and Computational Modeling.Brain sciences · 2025Review
- Studying the mechanisms of neurodegeneration:Frontiers in cellular neuroscience · 2025Review
- Live-cell visualization of tau aggregation in human neurons.Communications biology · 2024Article
- Application of Optogenetics in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2024Review
- Evaluating the inter-species transmission risk of amyloid beta peptide aggregates via ingestion.Alzheimer's research & therapy · 2024Article
- Article
- Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses.Aging and disease · 2024Review
- Optogenetics in Alzheimer's Disease: Focus on Astrocytes.Antioxidants (Basel, Switzerland) · 2023Review
- Zebrafish as a Model Organism for Studying Pathologic Mechanisms of Neurodegenerative Diseases and other Neural Disorders.Cellular and molecular neurobiology · 2023Review
- Using Optogenetics to Model Cellular Effects of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Simple models to understand complex disease: 10 years of progress fromFrontiers in neuroscience · 2023Review
- Precise modulation of embryonic development through optogenetics.Genesis (New York, N.Y. : 2000) · 2022Review
- The expanding role of split protein complementation in opsin-free optogenetics.Current opinion in pharmacology · 2022Review
- A light-inducible protein clustering system for in vivo analysis of α-synuclein aggregation in Parkinson disease.PLoS biology · 2022Article
- Optogenetics: implications for Alzheimer's disease research and therapy.Molecular brain · 2022Review
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The brains of Alzheimer's disease patients show a decrease in brain mass and a preponderance of extracellular Amyloid-β plaques. These plaques are formed by aggregation of polypeptides that are derived from the Amyloid Precursor Protein (APP). Amyloid-β plaques are thought to play either a direct or an indirect role in disease progression, however the exact role of aggregation and plaque formation in the aetiology of Alzheimer's disease (AD) is subject to debate as the biological effects of soluble and aggregated Amyloid-β peptides are difficult to separate in vivo. To investigate the consequences of formation of Amyloid-β oligomers in living tissues, we developed a fluorescently tagged, optogenetic Amyloid-β peptide that oligomerizes rapidly in the presence of blue light. We applied this system to the crucial question of how intracellular Amyloid-β oligomers underlie the pathologies of A. We use
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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.