ArticleScientific reports2018
Engineered Hsp70 chaperones prevent Aβ42-induced memory impairments in a Drosophila model of Alzheimer's disease.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 34 citations in OpenAlex.
- Context-dependent toxicity of human tau isoforms in a Drosophila tauopathy model.Biology open · 2026Article
- Differential expression of neuronal function genes follows a tissue-specific temporal dynamic during Deformed Wing Virus infection in honeybees.Scientific reports · 2026Article
- A J-domain protein enhances memory by promoting physiological amyloid formation inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Comparing In vitro Protein Aggregation Modelling Using Strategies Relevant to Neuropathologies.Cellular and molecular neurobiology · 2025Article
- Improved exposure of curcumin-loaded nanocapsules: drug quantification in LPS-inducedFrontiers in pharmacology · 2025Article
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- Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis.Nature communications · 2024Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Development and In Vivo Assessment of 4-Phenyltellanyl-7-chloroquinoline-loaded Polymeric Nanocapsules in Alzheimer's Disease Models.Brain sciences · 2023Article
- Review
- Closest horizons of Hsp70 engagement to manage neurodegeneration.Frontiers in molecular neuroscience · 2023Review
- Parkinson's Disease-Specific Autoantibodies against the Neuroprotective Co-Chaperone STIP1.Cells · 2022Article
- Mesenchymal stromal cells for the treatment of Alzheimer's disease: Strategies and limitations.Frontiers in molecular neuroscience · 2022Review
- Hsp70 affects memory formation and behaviorally relevant gene expression in Drosophila melanogaster.Cell stress & chaperones · 2021Article
- Regulation of neuroimmune processes by damage- and resolution-associated molecular patterns.Neural regeneration research · 2021Review
- Comprehensive Review on Alzheimer's Disease: Causes and Treatment.Molecules (Basel, Switzerland) · 2020Review
- PI3K activation prevents Aβ42-induced synapse loss and favors insoluble amyloid deposit formation.Molecular biology of the cell · 2020Article
- Genetic Dissection of Alzheimer's Disease UsingInternational journal of molecular sciences · 2020Review
- CCB is Involved in Actin-Based Axonal Transport of Selected Synaptic Proteins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
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3 authors at 2 institutions in 1 country.
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Abstract
Proteinopathies constitute a group of diseases in which certain proteins are abnormally folded leading to aggregation and eventual cell failure. Most neurodegenerative diseases belong to protein misfolding disorders and, among them, Alzheimer's disease (AD) is the most prevalent. AD is characterized by accumulation of the amyloid-β42 (Aβ42) peptide in the extracellular space. Hence, we genetically engineered a molecular chaperone that was selectively delivered to this cellular location. It has been reported that the heat shock protein 70 (Hsp70) binds Aβ42 preventing self-aggregation. Here, we employed two isoforms of the Hsp70, cytosolic and extracellular, to evaluate their potential protective effect against the memory decline triggered by extracellular deposition of Aβ42. Both Hsp70 isoforms significantly improved memory performance of flies expressing Aβ42, irrespective of their age or the level of Aβ42 load. Using olfactory classical conditioning, we established a Drosophila model of AD based on Aβ42 neurotoxicity and monitored memory decline through aging. The onset of the memory impairment observed was proportional to the cumulative level of Aβ42 in the Drosophila brain. These data support the use of this Drosophila model of AD to further investigate molecules with a protective activity against Aβ42-induced memory loss, contributing to the development of palliative therapies for AD.
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