ReviewExperimental neurology2015
Modeling the complex pathology of Alzheimer's disease in Drosophila.
Review in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 71 citations in OpenAlex.
- Review
- Exploring the versatility ofFly · 2025Review
- Modeling Alzheimer's Disease: A Review of Gene-Modified and Induced Animal Models, Complex Cell Culture Models, and Computational Modeling.Brain sciences · 2025Review
- Cephalic ganglia transcriptomics of the American cockroach Periplaneta americana (Blattodea: Blattidae).Journal of insect science (Online) · 2024Article
- Regulation of proteostasis by sleep through autophagy inLife science alliance · 2024Article
- Modeling the neuroimmune system in Alzheimer's and Parkinson's diseases.Journal of neuroinflammation · 2024Review
- Protein retention in the endoplasmic reticulum rescues Aβ toxicity in Drosophila.Neurobiology of aging · 2023Article
- Critical thinking of Alzheimer's transgenic mouse model: current research and future perspective.Science China. Life sciences · 2023Review
- Using Drosophila to identify naturally occurring genetic modifiers of amyloid beta 42- and tau-induced toxicity.G3 (Bethesda, Md.) · 2023Article
- Lipofuscin, amyloids, and lipid peroxidation as potential markers of aging in Daphnia.Biogerontology · 2023Article
- String/Cdc25 phosphatase is a suppressor of Tau-associated neurodegeneration.Disease models & mechanisms · 2023Article
- Aplysia Neurons as a Model of Alzheimer's Disease: Shared Genes and Differential Expression.Journal of molecular neuroscience : MN · 2022Article
- Dopamine, sleep, and neuronal excitability modulate amyloid-β-mediated forgetting in Drosophila.PLoS biology · 2021Article
- Deconstructing Alzheimer's Disease: How to Bridge the Gap between Experimental Models and the Human Pathology?International journal of molecular sciences · 2021Review
- Nutraceutical and Probiotic Approaches to Examine Molecular Interactions of the Amyloid Precursor Protein APP inInternational journal of molecular sciences · 2021Review
- From Combinations to Single-Molecule Polypharmacology-Cromolyn-Ibuprofen Conjugates for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2021Article
- Heat shock proteins and small nucleolar RNAs are dysregulated in a Drosophila model for feline hypertrophic cardiomyopathy.G3 (Bethesda, Md.) · 2021Article
- Pharmacological Treatment of Alzheimer's Disease: Insights fromInternational journal of molecular sciences · 2020Review
- Modeling Neurodegenerative Disorders inInternational journal of molecular sciences · 2020Review
- CHIP modulates APP-induced autophagy-dependent pathological symptoms in Drosophila.Aging cell · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the leading cause of dementia and the most common neurodegenerative disorder. AD is mostly a sporadic disorder and its main risk factor is age, but mutations in three genes that promote the accumulation of the amyloid-β (Aβ42) peptide revealed the critical role of amyloid precursor protein (APP) processing in AD. Neurofibrillary tangles enriched in tau are the other pathological hallmark of AD, but the lack of causative tau mutations still puzzles researchers. Here, we describe the contribution of a powerful invertebrate model, the fruit fly Drosophila melanogaster, to uncover the function and pathogenesis of human APP, Aβ42, and tau. APP and tau participate in many complex cellular processes, although their main function is microtubule stabilization and the to-and-fro transport of axonal vesicles. Additionally, expression of secreted Aβ42 induces prominent neuronal death in Drosophila, a critical feature of AD, making this model a popular choice for identifying intrinsic and extrinsic factors mediating Aβ42 neurotoxicity. Overall, Drosophila has made significant contributions to better understand the complex pathology of AD, although additional insight can be expected from combining multiple transgenes, performing genome-wide loss-of-function screens, and testing anti-tau therapies alone or in combination with Aβ42.
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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.