Transgenic Mouse Model of Tau Pathology in Astrocytes Leading to Nervous System Degeneration
Open accessAbstract
Filamentous tau inclusions in neurons and glia are neuropathological hallmarks of sporadic and familial tauopathies. Because tau gene mutations are pathogenic for the autosomal dominant tauopathy “frontotemporal dementia and parkinsonism linked to chromosome 17,” tau abnormalities are implicated directly in the onset and/or progression of disease. Although filamentous tau aggregates are acknowledged to play roles in degenerative mechanisms resulting in neuron loss, the contributions of glial tau pathology to neurodegeneration remain essentially unexplored. To begin to elucidate the role of glial pathology in tauopathies, we generated a transgenic (Tg) mouse model of astrocytic tau pathology by expressing the human tau protein driven by the glial fibrillary acidic protein (GFAP) promoter. Whereas endogenous tau was not detected in astrocytes of control mice, in GFAP/tau Tg mice there was robust astrocytic tau expression that was associated with a redistribution of the GFAP network. Subsequently, there was an age-dependent accumulation of tau pathology in astrocytes that was Gallyas and variably thioflavine S positive as observed in many tauopathies. The tau pathology in these Tg mice was abnormally phosphorylated, ubiquitinated, and filamentous, and the emergence of this pathology coincided with accumulation of insoluble tau protein. Furthermore, in regions with robust astrocytic tau pathology, there was mild blood- brain barrier disruption, induction of low-molecular-weight heat shock proteins, and focal neuron degeneration. Thus, these Tg mice recapitulate key features of astrocytic pathology observed in human tauopathies and demonstrate functional consequences of this pathology including neuron degeneration in the absence of neuronal tau inclusions.
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Accumulation of tau in astrocytes alters astrocytic function, induces neuronal degeneration and promotes cell death through serial degenerative events such as BBB collapse and expression of low-molecular-weight heat shock proteins.
“Accumulation of tau in astrocytes alters astrocytic function, induces neuronal degeneration and promotes cell death through a serial degenerative events, such as boosting blood-brain barrier (BBB) collapse, and inducing expression of heat shock proteins with low molecular weight [228, 434, 436, 437].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [434]
Phosphorylation, fibrosis and asymmetric accumulation of tau in astrocytes increase with age in mice expressing P301L tau.
“Phosphorylation, fibrosis and asymmetric accumulation of tau in astrocytes increased with age in mice expressing P301L tau [434].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [434]
In mice expressing P301L human tau under an astrocyte-specific promoter, tau accumulation in astrocytes is followed by neuronal degeneration.
“Finally, neurofilament staining revealed ballooned neurons and axonal degeneration in areas with abundant tau pathology [126].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [126]
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- Authors
- Forman, M. S., Lal, D., Zhang, B., Dabir, D. V., Swanson, E., Lee, V. M.-Y., & Trojanowski, J. Q.
- Affiliations
- University of Pennsylvania (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-04-06
- Volume
- 25
- Issue
- 14
- Pages
- 3539-3550
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6725385
- OpenAlex
- W2027582763
- Cited by
- 198
- References
- 57
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 15 · 2023: 10 · 2022: 8 · 2021: 15 · 2020: 14 · 2019: 16 · 2018: 12 · 2017: 18 · 2016: 8 · 2015: 11 · 2014: 10 · 2013: 6 · 2012: 2
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Pennsylvania
- National Institute on Aging (P01 AG-17586, K08 AG20073, P01AG017586, AG17586, K08AG020073)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- tauopathy, transgenic mouse model, glial fibrillary acidic protein promoter, tau phosphorylation, tau aggregation, blood-brain barrier disruption, heat shock proteins, neuron degeneration, neurodegeneration
- MeSH terms
- Age Factors, Animals, Astrocytes, Axons, Blood-Brain Barrier, Brain, Disease Models, Animal, Humans, Immunohistochemistry, Mice, Transgenic, Nerve Degeneration, Blotting, Western, Gene Expression, Microscopy, Immunoelectron, Neurofibrillary Tangles, tau Proteins, Neurofilament Proteins, Ubiquitin, Green Fluorescent Proteins, Mice
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