Tauopathy in Drosophila : Neurodegeneration Without Neurofibrillary Tangles
Abstract
The microtubule-binding protein tau has been implicated in the pathogenesis of Alzheimer's disease and related disorders. However, the mechanisms underlying tau-mediated neurotoxicity remain unclear. We created a genetic model of tau-related neurodegenerative disease by expressing wild-type and mutant forms of human tau in the fruit fly Drosophila melanogaster. Transgenic flies showed key features of the human disorders: adult onset, progressive neurodegeneration, early death, enhanced toxicity of mutant tau, accumulation of abnormal tau, and relative anatomic selectivity. However, neurodegeneration occurred without the neurofibrillary tangle formation that is seen in human disease and some rodent tauopathy models. This fly model may allow a genetic analysis of the cellular mechanisms underlying tau neurotoxicity.
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Several invertebrate and vertebrate transgenic animal models have shown that tau can induce neurodegeneration and apoptosis.
“Several invertebrate and vertebrate transgenic animal models have shown that tau can induce neurodegeneration and apoptosis (43–46).”
From Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation (2011) · cites this paper as [45]
Pan-neuronal transgenic expression of an FTDP-17 mutant form of human tau, tauR406W, in Drosophila causes progressive neurodegeneration and provides a well-characterized in vivo genetic model of tau neurotoxicity.
“Pan-neuronal transgenic expression of an FTDP-17 mutant form of human tau, tauR406W, in Drosophila causes progressive neurodegeneration and provides a well-characterized in vivo genetic model of tau neurotoxicity7,15,16.”
From Tau promotes neurodegeneration through global chromatin relaxation (2014) · cites this paper as [15]
Drosophila models of human tauopathy have progressive, age-associated neuronal death, a shortened lifespan, and decreased locomotor activity.
“Drosophila models of human tauopathy have progressive, age-associated neuronal death, a shortened lifespan, and decreased locomotor activity10,11.”
From Pathogenic tau-induced piRNA depletion promotes neuronal death through transposable element dysregulation in neurodegenerative tauopathies (2018) · cites this paper as [11]
Human tau expression in the adult Drosophila brain significantly alters levels of transposable element transcripts.
“Beginning with a simple model of tauopathy in Drosophila melanogaster11, we report significantly altered levels of transposable element transcripts as a consequence of human tau expression in the adult brain.”
From Pathogenic tau-induced piRNA depletion promotes neuronal death through transposable element dysregulation in neurodegenerative tauopathies (2018) · cites this paper as [11]
Neuronal loss appears to be independent of tangle formation in some transgenic mouse models.
“However, neuronal loss appears to be independent of tangle formation in some transgenic mouse models (12)(13)(14).”
Formation of fibrils or detergent-insoluble aggregates are not detected in the presence or absence of Aβ in Drosophila models.
“Formation of fibrils or detergent-insoluble aggregates are not detected in the presence or absence of Aβ [58, 59]”
Drosophila models expressing human tau recapitulate key features of human tauopathies, including progressive neurodegeneration and phosphorylation at AD-related sites via conserved kinases.
“Drosophila models expressing human tau recapitulate key features of human tauopathies, including progressive neurodegeneration and phosphorylation at AD-related sites via conserved kinases [41, 44, 53, 59–63].”
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- Authors
- Wittmann, C. W., Wszolek, M. F., Shulman, J. M., Salvaterra, P. M., Lewis, J., Hutton, M., & Feany, M. B.
- Affiliations
- Brigham and Women's Hospital (US)
- Beckman Research Institute (US)
- Mayo Clinic (US)
- Department of Pathology, Division of Neuropathology, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, Room 514, Boston, MA 02115, USA.
- Venue
- Science
- Published
- 2001-07-27
- Volume
- 293
- Issue
- 5530
- Pages
- 711-714
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2038120434
- Cited by
- 939
- References
- 1
- Citations by year
- 2026: 24 · 2025: 36 · 2024: 35 · 2023: 41 · 2022: 28 · 2021: 46 · 2020: 45 · 2019: 37 · 2018: 31 · 2017: 46 · 2016: 39 · 2015: 34 · 2014: 37 · 2013: 35 · 2012: 38
- FWCI
- 19.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- tauopathy, tau protein, neurodegeneration, Drosophila melanogaster, Alzheimer's disease, neurofibrillary tangles, tau accumulation, neurotoxicity mechanisms
- MeSH terms
- Acetylcholine, Aging, Animals, Brain, Disease Models, Animal, Drosophila melanogaster, Humans, Mutation, Nerve Degeneration, Nerve Endings, Neurons, Phosphorylation, Vacuoles, Neurofibrillary Tangles, tau Proteins, Neuropil, Neurodegenerative Diseases, Animals, Genetically Modified
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