Accelerated tau pathology with synaptic and neuronal loss in a novel triple transgenic mouse model of Alzheimer’s disease
Open accessAbstract
There is pivotal evidence that tau pathology can be triggered by amyloid-β (Aβ) pathology in experimental systems. On the other side, studies on human brain specimen have elucidated that tau pathology may occur before amyloid pathology is present indicating that in principle tau pathology could also trigger Aβ aggregation. To address this question, we have crossed 5XFAD mice coexpressing human mutant APP695 with the Swedish, Florida, and London mutations and human mutant presenilin-1 (PS1) with the M146L and L286V mutations with the PS19 model overexpressing human mutant tau with the P301S mutation. The resulting triple transgenic model 5XFAD/PS19 has been characterized at 3 and 9 months of age. A dramatic aggravation of hyperphosphorylated tau pathology together with a dramatically increased inflammatory response and a loss of synapses and hippocampal CA1 neurons in aged 5XFAD/PS19 mice were observed. Extracellular amyloid deposits were unaltered. These data support the assumption of tau pathology being downstream of amyloid pathology, suggesting that both pathologies together trigger the severe neuron loss in the hippocampus in the 5XFAD/PS19 mouse model.
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In 5xFAD/PS19 mice, co-expression of Tau led to deficits in basal synaptic transmission, spatial memory deficits, increased neuroinflammation, robust hippocampal atrophy, and severe loss of neurons in the hippocampal CA1 layer.
“Co-expression of Tau lead to deficits in basal synaptic transmission, as well as spatial memory deficits [57] and increased neuroinflammation [56]. Of note, 5xFAD/PS19 mice presented with robust hippocampal atrophy and severe loss of neurons in the hippocampal CA1 layer [56,57].”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [56]
The study used 9-month-old animals, when each model exhibits robust amyloid and/or tau pathology, and included equal numbers of males and females.
“We used 9‐month‐old animals, when each model exhibits robust amyloid and/or tau pathology, 11 , 12 , 43 and included equal numbers of males and females.”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [43]
Synaptic dysfunction is a hallmark of AD and has been reported in both combined pathology mouse models and human AD brains.
“Synaptic dysfunction is a hallmark of AD and has been reported in both combined pathology mouse models and human AD brains. 43 , 58 , 59”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [43]
The tau pathology does not appear to increase Aβ deposition.
“The tau pathology does not appear to increase Aβ deposition (Saul et al., 2013; Chabrier et al., 2014; Heraud et al., 2014; Stancu et al., 2014; Chen et al., 2016; Kang et al., 2021); indeed, in some cases it accelerates removal of Aβ (Chen et al., 2016).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saul et al., 2013
Our results for Aβ and MAPT pathologies are generally consistent with prior observations using crosses of APP over-expression mouse lines and MAPT over-expression mouse models.
“Our results for Aβ and MAPT pathologies are generally consistent with prior observations using crosses of APP over-expression mouse lines and MAPT over-expression mouse models (Saul et al., 2013; Chabrier et al., 2014; Heraud et al., 2014; Stancu et al., 2014; Chen et al., 2016; Kang et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saul et al., 2013
Over-expression models consistently observe that the presence of Aβ pathology enhances the accumulation of MAPT pathology, neurodegeneration and cognitive loss.
“These over-expression models consistently observe that the presence of Aβ pathology enhances the accumulation of MAPT pathology, neurodegeneration and cognitive loss (Saul et al., 2013; Chabrier et al., 2014; Heraud et al., 2014; Stancu et al., 2014; Chen et al., 2016; Kang et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saul et al., 2013
The same studies indicate that the presence of MAPT pathology either does not change the accumulation of Aβ pathology or decreases it.
“These same studies indicate that the presence of MAPT pathology either does not change the accumulation of Aβ pathology or decreases it (Saul et al., 2013; Chabrier et al., 2014; Heraud et al., 2014; Stancu et al., 2014; Chen et al., 2016; Kang et al., 2021), with only one initial study suggesting that MAPT pathology increases Aβ pathology (Ribe et al., 2005).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saul et al., 2013
No evidence for increased Aβ pathology was evident in 5XFAD/PS19 mice at either 3 or 9 months of age.
“Using the same line of P301S tau transgenic mice, a trend towards a higher extracellular amyloid plaque load was detected in PDAPP/Tau bigenic mice [8], while no evidence for increased Aβ pathology was evident in 5XFAD/PS19 mice at either 3 or 9 months of age [9].”
From Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau (2021) · cites this paper as [9]
Findings in models harboring transgenic Aβ peptides in the absence of APP overexpression strikingly contrast the obvious exacerbation of tau pathology observed in tau transgenic mice when crossed with mouse models of AD overexpressing mutant APP.
“These findings in models harboring transgenic Aβ peptides in the absence of APP overexpression strikingly contrast the obvious exacerbation of tau pathology observed in tau transgenic mice when crossed with mouse models of AD overexpressing mutant APP [7,8,9,10,11,12,13,36].”
From Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau (2021) · cites this paper as [9]
A significantly decreased number of CA1 pyramidal cells has been detected in 9-month-old 5XFAD/PS19 mice in comparison to their parental single transgenic 5XFAD or PS19 lines.
“With regard to hippocampal neuron loss, a significantly decreased number of CA1 pyramidal cells has been detected in 9-month-old 5XFAD/PS19 mice in comparison to their parental single transgenic 5XFAD or PS19 lines [9].”
From Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau (2021) · cites this paper as [9]
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- Authors
- Saul, A., Sprenger, F., Bayer, T. A., & Wirths, O.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2013-11
- Volume
- 34
- Issue
- 11
- Pages
- 2564-2573
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2023771355
- Semantic Scholar
- 6041f4e5569f349f203bae1c5556b12ef753c2c3
- Cited by
- 85
- References
- 42
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 8 · 2023: 5 · 2022: 2 · 2021: 10 · 2020: 18 · 2019: 4 · 2018: 3 · 2017: 6 · 2016: 8 · 2015: 4 · 2014: 6 · 2013: 2
- FWCI
- 4.09
- Type
- journal article
- Language
- en
- Open access
- Licence
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, cc-by)
- Funders
- Alzheimer Forschung Initiative
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- tau pathology, Alzheimer's disease, amyloid-beta, 5xFAD mice, PS19 mice, triple transgenic mouse model, hyperphosphorylated tau, synaptic loss, neuronal loss, CA1 pyramidal neurons, neuroinflammation, presenilin 1 mutations, amyloid-beta aggregation
- MeSH terms
- Age Factors, Alzheimer Disease, Analysis of Variance, Animals, Astrocytes, Disease Models, Animal, Glial Fibrillary Acidic Protein, Hippocampus, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Nerve Degeneration, Neurons, Synapses, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Mice, Presenilin-1
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