Spatial memory deficiency early in 6xTg Alzheimer’s disease mouse model
Open accessAbstract
Alzheimer’s disease (AD) is mainly characterized by the deposition of extracellular amyloid plaques and intracellular accumulation of neurofibrillary tangles (NFTs). While the recent 5xFAD AD mouse model exhibits many AD-related phenotypes and a relatively early and aggressive amyloid β production, it does not show NFTs. Here, we developed and evaluated a novel AD mouse model (6xTg-AD, 6xTg) by crossbreeding 5xFAD mice with mice expressing mutant (P301L) tau protein (MAPT). Through behavioral and histopathological tests, we analyzed cognitive changes and neuropathology in 6xTg mice compared to their respective parental strains according to age. Spatial memory deficits occurred in 6xTg mice at 2 months of age, earlier than they occurred in 5xFAD mice. Histopathological data revealed aggressive Aβ42 and p-tau accumulation in 6xTg mice. Microglial activation occurred in the cortex and hippocampus of 6xTg mice beginning at 2 months. In 6xTg model mice, the synaptic loss was observed in the cortex from 4 months of age and in the hippocampus from 6 months of age, and neuronal loss appeared in the cortex from 4 months of age and in the hippocampus 6 months of age, earlier than it is observed in the 5xFAD and JNPL3 models. These results showed that each pathological symptom appeared much faster than in their parental animal models. In conclusion, these novel 6xTg-AD mice might be an advanced animal model for studying AD, representing a promising approach to developing effective therapy.
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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 [12]
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- Authors
- Kang, S., Kim, J., & Chang, K.-A.
- Affiliations
- Gachon University (KR)
- Corresponding author
- Chang, Keun-A
- Venue
- Scientific Reports
- Published
- 2021-01-14
- Volume
- 11
- Issue
- 1
- Pages
- 1334-1334
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC7809274
- OpenAlex
- W3125014734
- Cited by
- 39
- References
- 38
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 9 · 2023: 15 · 2022: 6 · 2021: 4
- FWCI
- 5.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Reserach Foundation of Korea (2020M3A9E4104384)
- National Research Foundation of Korea (2016M3C7A1914451)
- 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
- Alzheimer's disease, 5xFAD mice, P301L tau, MAPT, amyloid-beta 42, phosphorylated tau, microglial activation, synaptic loss, neuronal loss, spatial memory impairment, cognitive impairment, amyloid plaques, neurofibrillary tangles, hippocampus
- MeSH terms
- Alzheimer Disease, Animals, Brain, Cognition, Disease Models, Animal, Memory Disorders, Mice, Transgenic, tau Proteins, Mutation, Missense, Mice
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