ReviewBrain structure & function2010
Transgenic Drosophila models of Alzheimer's disease and tauopathies.
Review in Brain structure & function, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 108 citations in OpenAlex.
- Progressive behavioral and cognitive decline inbioRxiv : the preprint server for biology · 2026Article
- 2-(Arylamino)thiazol-4(5H)-ones Mitigate Oxidative Stress and Confer Neuroprotection in Cellular andInternational journal of molecular sciences · 2026Article
- Neuroprotective potential of marine-derived polysaccharide against Aβ42-induced toxicity in a Drosophila Alzheimer's disease model.Molecular biology reports · 2026Article
- Role of Oxidative Stress in Human Neurodegenerative Pathologies: Lessons from theCurrent topics in medicinal chemistry · 2026Review
- Examining the role of antioxidant supplementation in mitigating oxidative stress markers in Alzheimer's disease: a comprehensive review.Inflammopharmacology · 2025Review
- The spectrum-efficacy correlation of Kai-Xin-San for cognition of AβFrontiers in pharmacology · 2025Article
- Recent Advances in Targeting Transition Metals (Copper, Iron, and Zinc) in Alzheimer's Disease.Molecular neurobiology · 2024Review
- Using Drosophila to identify naturally occurring genetic modifiers of amyloid beta 42- and tau-induced toxicity.G3 (Bethesda, Md.) · 2023Article
- Big tau aggregation disrupts microtubule tyrosination and causes myocardial diastolic dysfunction: from discovery to therapy.European heart journal · 2023Article
- Current progress of cerebral organoids for modeling Alzheimer's disease origins and mechanisms.Bioengineering & translational medicine · 2023Review
- Drug discovery from natural products - Old problems and novel solutions for the treatment of neurodegenerative diseases.Journal of pharmaceutical and biomedical analysis · 2022Review
- Antioxidants in Alzheimer's Disease: Current Therapeutic Significance and Future Prospects.Biology · 2022Review
- DYRK1a Inhibitor Mediated Rescue ofFrontiers in pharmacology · 2022Article
- Diplazium esculentum (Retz.) Sw. reduces BACE-1 activities and amyloid peptides accumulation in Drosophila models of Alzheimer's disease.Scientific reports · 2021Article
- Dopamine, sleep, and neuronal excitability modulate amyloid-β-mediated forgetting in Drosophila.PLoS biology · 2021Article
- A Two-Clone Approach to Study Signaling Interactions among Neuronal Cells in a Pre-clinical Alzheimer's Disease Model.iScience · 2020Article
- Miro, a Rho GTPase genetically interacts with Alzheimer's disease-associated genes (Biology open · 2020Article
- PI3K activation prevents Aβ42-induced synapse loss and favors insoluble amyloid deposit formation.Molecular biology of the cell · 2020Article
- The Erythrocytic Hypothesis of Brain Energy Crisis in Sporadic Alzheimer Disease: Possible Consequences and Supporting Evidence.Journal of clinical medicine · 2020Review
- A Positive Feedback Loop of Hippo- and c-Jun-Amino-Terminal Kinase Signaling Pathways Regulates Amyloid-Beta-Mediated Neurodegeneration.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common form of senile dementia. Aggregation of the amyloid-beta42 peptide (Abeta42) and tau proteins are pathological hallmarks in AD brains. Accumulating evidence suggests that Abeta42 plays a central role in the pathogenesis of AD, and tau acts downstream of Abeta42 as a modulator of the disease progression. Tau pathology is also observed in frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17) and other related diseases, so called tauopathies. Although most cases are sporadic, genes associated with familial AD and FTDP-17 have been identified, which led to the development of transgenic animal models. Drosophila has been a powerful genetic model system used in many fields of biology, and recently emerges as a model for human neurodegenerative diseases. In this review, we will summarize key features of transgenic Drosophila models of AD and tauopathies and a number of insights into disease mechanisms as well as therapeutic implications gained from these models.
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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.