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Alzheimer’s disease AD animal model

Alzheimer’s disease AD animal model

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Alzheimer's disease
Psychiatric & neurological disease models

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Experimental results

Experimental results

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Alzheimer's disease

Introduction to the AD Mouse Model

Alzheimer’s disease (AD) is a neurodegenerative disorder that predominantly affects the elderly, ranking fourth among causes of death worldwide, behind cancer, cardiovascular disease, and stroke. The condition progressively worsens with age; in its early stages, patients typically exhibit memory impairment, which gradually advances to severe dementia, accompanied by deficits in language, cognitive function, visuospatial abilities, and executive functions. At present, clinical practice still lacks a curative treatment, resulting in prolonged recovery periods and a generally poor prognosis. Developing effective interventions and therapies to extend survival and enhance quality of life has thus become a significant challenge. Experimental animals serve as crucial tools in disease research and drug development; establishing stable and reliable AD animal models lays a solid experimental foundation for investigating the etiological factors and underlying mechanisms of the disease.

Advantages of Aniphe BioLab’s AD Mouse Model Platform Services

Leveraging a well-established AD model‑generation platform, we offer multiple modeling approaches and implement rigorous batch‑to‑batch quality control and inclusion criteria, providing a stable and reliable in vivo solution for your drug discovery and preclinical efficacy evaluation.

Comprehensive model coverage

Multiple models available

It supports multiple AD modeling approaches, including transgenic, chemically induced, and surgically induced methods, and can be tailored to meet the needs of various research directions and experimental designs.
Standardization of the modeling process

The model is stable and controllable.

Based on established modeling expertise, pathological features and behavioral phenotypes can be consistently reproduced, thereby minimizing inter‑batch variability.
Multidimensional Evaluation System

Strictly Selected Inclusion Criteria

Experimental animals from the same batch were rigorously screened to minimize variability in baseline parameters, thereby ensuring the statistical power of the experimental data.
Adapted for multi-cycle studies

Multi-stage disease course adaptation

It can provide AD models at different stages of disease progression, supporting end-to-end pharmacological efficacy evaluation—from early-stage intervention to mid- and late-stage pathological assessment.
Standardization of Data Delivery

Efficient Delivery Services

We provide rapid, reliable model preparation and comprehensive evaluation services to help projects advance efficiently.
Modeling cycle

4–6 weeks

1  Laboratory animals

Animal models induced by physical or pharmacological methods, naturally aged animals, the senescence-accelerated mouse strains SAMP8 and SAMP10, APP/PS1 transgenic mice, APP/PS1/Tau transgenic mice, and 5×FAD transgenic mice.

1  Positive drug

These primarily include cholinesterase inhibitors (such as donepezil), NMDA receptor antagonists (such as memantine), investigational antibody‑based therapies targeting Aβ and tau (e.g., lecanemab), and natural antioxidants.

1  Application areas

Animal models are extensively employed in research on the pathogenesis of Alzheimer’s disease, in vivo screening and efficacy evaluation of candidate drugs, assessment of novel therapeutic strategies—including gene and cell therapies—and translational medicine studies, thereby providing critical support for the development of new AD therapeutics and preclinical validation.

Experimental results

Immunohistochemical staining results

The figure compares the brain Aβ protein expression levels between the normal control group (NC) and 6-month-old APP/PS1/Tau model mice:

In the normal control (NC) group, Aβ-positive signals in the brain were very sparse, with faint staining background and no obvious Aβ deposition plaques.

At 6 months of age, APP/PS1/Tau model mice exhibit a marked increase in brownish‑brown Aβ‑positive staining signals in the brain, indicating that the model has successfully developed the core pathological hallmark of Alzheimer’s disease—β‑amyloid deposition—and that the model‑generation protocol is effective.

 

 

Therapeutic Outcomes of Memantine

01 Morris Water Maze Test

Using 3xTg‑AD composite‑pathology mice at 6, 9, and 15 months of age, we conducted Morris water maze testing following a 3‑month memantine intervention. The results showed that, with advancing age, 3xTg transgenic mice exhibited progressive decline in spatial learning and memory; long‑term memantine administration significantly shortened escape latency and improved platform‑related memory retention, with the most pronounced cognitive‑enhancing effects observed in 15‑month‑old aged mice bearing severe pathology. By contrast, memantine had no significant effect on normal wild‑type mice.

 

 

02 Western Blot Analysis

Validation of memantine’s intervention effects on tau pathology in 3xTg mice: the drug does not alter total Tau expression but significantly reduces pathogenic phosphorylated Tau species, including AT8, AT100, and PHF‑1. Mechanistically, it suppresses Tau phosphorylation by increasing the activity of the inactive form of GSK‑3β, thereby effectively alleviating intraneuronal tau tangle pathology.

 

 

03 ELISA Quantification and Immunohistochemical Results for Aβ in Brain Tissue

Quantitative ELISA and Aβ immunohistochemistry confirmed that memantine significantly reduces both soluble toxic Aβ oligomers and insoluble amyloid plaque burden in the brains of 3xTg‑AD mice; moreover, the older the animals and the more severe their baseline Aβ pathology, the more pronounced the drug’s ameliorative effect on these deposits.

 

 

References: Memantine Improves Cognition and Reduces Alzheimer’s-Like Neuropathology in Transgenic Mice.

 

Different modeling methods for Alzheimer’s disease models

Dementia rat model induced by fornix–hippocampal commissure transection

Animal selection: Male rats weighing 250–300 g.

Procedure: Anesthetize rats, perform a craniotomy to transect the fornix–hippocampal commissure, and resect either unilaterally or bilaterally.

Model characteristics: This model effectively simulates cholinergic system dysfunction in the forebrain of Alzheimer’s disease (AD) and allows for the assessment of drug‑induced restoration of neuronal function, making it an important preclinical pharmacodynamic tool for AD research. However, it lacks the hallmark neuropathological features of AD and is characterized solely by impairments in learning and memory; moreover, the lesion extent is quite extensive, so this model is now used less frequently.

Oxoglutamic acid–induced dementia model

Animal selection: male rats, weighing 250–300 g.

Experimental procedure: Following anesthesia, a craniotomy was performed and IBO was injected; in the sham‑operation group, an equivalent volume of PBS was injected into the same site.

Model characteristics: Following IBO injection, rats exhibit biting of the forelimbs; in the dark–light avoidance test, the latency to enter the dark compartment is significantly reduced from days 1 to 35 post‑surgery, and by day 30, a marked decrease in 5‑HT levels is observed in hippocampal and thalamic tissues. This model can replicate the cholinergic deficit in the basal forebrain seen in Alzheimer’s disease, while hippocampal ChAT activity remains unaffected. It is one of the primary animal models used for preclinical pharmacodynamic studies.

Scopolamine-Induced Dementia Model

Experimental procedure: SCOP was administered via intraperitoneal injection, inducing cholinergic system dysfunction in the animals and thereby impairing their cognitive performance.

Model characteristics: The construction method is simple and cost-effective; the model does not directly induce cholinergic neuronal loss, exhibits rapid recovery, and is suitable for early-stage drug screening.

D-galactose model

Animal selection: adult rats or mice

Experimental protocol: Mice were administered D-galactose in saline by daily subcutaneous or intraperitoneal injection for 40 consecutive days; rats received subcutaneous injections for 6–7 consecutive weeks.

Model characteristics: The model is quick to construct, cost-effective, and yields reliable, stable results; its pathological changes closely resemble those observed in clinical AD patients, making it widely used in anti‑aging research within China.

Aβ injection–induced dementia model

Animal selection: SD rats (both sexes), weighing 200–300 g; or male ICR mice, weighing 18–20 g.

Experimental procedure: Anesthetize the experimental mice, inject Aβ directly into the cerebral ventricles, and house them individually in cages until they have fully regained consciousness.

Model characteristics: Acute intracerebral injection of Aβ in animals induces behavioral deficits and memory impairments resembling those seen in Alzheimer’s disease, including impaired active and passive avoidance responses and reduced spatial discrimination. Additionally, the model exhibits neuronal loss and degeneration in the cortex and hippocampus, subcortical cerebral amyloid angiopathy, and Aβ deposition. It is well suited for investigating the effects of AD‑targeted therapeutics on Aβ aggregation or deposition, neurotoxicity, and microglial inflammatory responses, making it an important preclinical pharmacodynamic evaluation model.