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Mouse Classroom | With so many AD models, what are the differences?

Introduction:

Research on Alzheimer’s disease (AD) has long been a major focus, and for more than a decade, our efforts to unravel this condition have never ceased. In June of this year, an article published in Nature titled “Faulty autolysosome acidification in Alzheimer’s disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques” sparked widespread debate, offering new insights and avenues for reflection on the pathogenic mechanisms of AD.

Currently, the animal models of Alzheimer’s disease (AD) on the market primarily rely on several transgenic mouse strains, including the APP/Ps1 mouse (commonly referred to as the “double‑transgenic” model), the 3×Tg mouse (often called the “triple‑transgenic” model), and the 5×FAD mouse. These models exhibit variable disease phenotypes depending on their genetic background and the specific age at which they are studied. Today, we will provide a detailed overview of the phenotypic characteristics of these different AD mouse models.

Today, we’ll provide a detailed overview of the phenotypic characteristics of various AD‑model mice.

Double-transgenic mice—APP/PS1 mice (C57BL/6 background)

Gene: APP, PSEN1

Mutant gene: APP KM670/671NL (Swedish), PSEN1: deltaE9

Modifier gene: APP: transgenic; PSEN1: transgenic

Neuropathology: Around 4 months of age, amyloid plaques begin to appear in the cerebral cortex, and by 6 months, they also emerge in the hippocampus. Glial proliferation and neuronal dystrophy are associated with these plaques. Amyloid angiopathy has been observed in the retina.

Behavioral/Cognitive Science: At 6 months, hyperactivity was pronounced. Deficits in the Morris water maze emerged between 6 and 10 months and worsened with age.

Double-transgenic mice—APP/PS1 mice (C57BL/6; C3H background)

Gene: APP, PSEN1

Mutant gene: APP KM670/671NL (Swedish), PSEN1: deltaE9

Modifier gene: APP: transgenic; PSEN1: transgenic

Neuropathology: At 6 months, Aβ deposition was observed sporadically; by 9 months, hippocampal and cortical plaques were abundant; and by 12 months, plaque burden continued to increase. No neurofibrillary tangles were present. Synaptic markers were reduced, while complement immunoreactivity was elevated.

Behavioral/Cognitive Science: Cognitive impairments (such as deficits in spatial memory and contextual memory). Alterations in spontaneous behaviors (e.g., nest building, burrowing).

Three-transgenic mice — 3×Tg mice

Gene: APP, PSEN1, MAPT

Mutant gene: APP KM670/671NL (Swedish), MAPT P301L, PSEN1 M146V

Modifier gene: APP: transgenic; PSEN1: transgenic; MAPT: transgenic

Neuropathology: Age-related progressive neuropathology, including plaques and tangles.

Extracellular Aβ deposition in the frontal cortical neurons occurs at 6 months and becomes more widespread by 12 months. Tau pathology is absent at 6 months but becomes evident by 12 months. Synaptic dysfunction, including deficits in long-term potentiation (LTP), precedes both amyloid plaques and neurofibrillary tangles.

Behavioral/Cognitive Science: Four months of cognitive impairment. The deficit initially manifests as a memory/retrieval impairment rather than a learning deficit, and it precedes the emergence of plaques and tangles. Deficits are observed in spatial and contextual paradigms. Clearance of intraneuronal Aβ via immunotherapy can reverse early cognitive deficits in hippocampus‑dependent tasks.

Five-transgenic mice—5×FAD mice (B6SJL background)

Gene: APP, PSEN1

Mutant gene: APP KM670/671NL (Swedish), APP I716V, APP V717I, PSEN1 M146L (A>C), PSEN1 L286V

Modifier gene: APP: transgenic; PSEN1: transgenic

Neuropathology: Amyloid pathology, including amyloid plaques, begins to emerge after two months. Prior to amyloid deposition, Aβ accumulates within neurons. Glial cell activation and synaptic degeneration also occur. Neuronal loss is observed in layer V and the subplate of the cortex. Neurofibrillary tangles are present.

Behavioral/Cognitive Science: Age‑dependent memory deficits encompass spatial memory, stress‑related memory, and memory consolidation. It is a motor‑performance phenotype.

Five-transgenic mice—5×FAD (C57BL/6 background)

Gene: APP, PSEN1

Mutant gene: APP KM670/671NL (Swedish), APP I716V, APP V717I, PSEN1 M146L (A>C), PSEN1 L286V

Modifier gene: APP: transgenic; PSEN1: transgenic

Neuropathology: Amyloid pathology, including amyloid plaques, begins to emerge at 2 months. Prior to amyloid deposition, Aβ accumulates within neurons. Glial cell activation and synaptic degeneration also occur. Neuronal loss is observed in layer V of the cortex.

Behavioral/Cognitive Science: Age-dependent memory deficits, motor phenotypes, and reduced anxiety.

Ailinfei Laboratory has established a systematic and comprehensive library of AD mouse models.

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Morris water maze, novel object recognition box, elevated plus-maze, forced swim test box, and open-field apparatus, among others. Small Animal Behavior Analysis and Testing Platform ；

Transcriptomics, proteomics, metabolomics Multi-omics Integrated Data Processing Platform ；

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Small-animal stereotaxic injector, respiratory anesthetics, etc. Surgical platform ；

Small-animal CT, ultrasound imaging, in vivo imaging, and more Small Animal Imaging Platform 。

Welcome to inquire and place your order!

That concludes this episode of Rat Classroom.

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