All
  • All
  • Insight
  • Research Services
  • Preclinical CRO
  • Animal Resource Bank
CN
中文 English

Allergic encephalomyelitis animal model of AE

Allergic encephalomyelitis animal model of AE

Explore more

Encephalomyelitis
Psychiatric & neurological disease models

On this page

Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Model Construction

Model Construction

Model Evaluation

Model Evaluation

Publish an article

View more

Encephalomyelitis

Introduction to the AE Mouse Model

The experimental autoimmune encephalomyelitis (EAE) mouse model is currently recognized as an ideal animal model for mimicking human multiple sclerosis (MS) and serves as a crucial tool in the field of neuroimmunology for studying autoimmune demyelinating diseases. At its core, this model relies on antigen‑induced activation of the adaptive immune system mediated by CD4⁺ T cells, leading to chronic inflammatory damage in the central nervous system. Its hallmark pathological features include perivascular mononuclear cell infiltration in small vessels of the brain and spinal cord, widespread loss of myelin sheaths, along with axonal injury and neurological dysfunction—patterns that closely mirror the pathogenesis, disease progression, and clinical manifestations of human MS. Owing to its well‑established modeling protocol, stable pathological phenotype, and comprehensive evaluation framework, the EAE mouse model has been extensively employed in investigating the etiology and pathogenic mechanisms of MS, screening candidate therapeutics, optimizing treatment strategies, and conducting preclinical efficacy assessments, thereby providing essential in vivo experimental support for advancing the development of novel MS therapies.

AE Bio’s Mouse Model Platform Service Advantages

Leveraging established expertise in AE model development and a standardized evaluation framework, we provide a robust and reliable in vivo solution for the discovery and preclinical assessment of novel therapeutics for neuroimmune disorders such as multiple sclerosis.

Comprehensive model coverage

The model is stable and controllable.

Mature modeling methods can reliably induce autoimmune inflammation and demyelination in the central nervous system, with excellent phenotypic reproducibility.

Standardization of the modeling process

Quality Control Specifications for the Same Batch

Random sampling based on body weight, baseline neurological function, and other indicators ensures that the animals are homogeneous in condition prior to enrollment.

Multidimensional Evaluation System

Strictly Selected Inclusion Criteria

Control for baseline differences among animals within the same batch to ensure the statistical power of the experimental data.

Adaptable to multi-cycle studies

Multidimensional evaluation system

It provides neurological function scoring, clinical symptom monitoring, and detection of key pathological markers, enabling a comprehensive assessment of drug efficacy.

Standardization of Data Delivery

Efficient Delivery Support

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

Modeling cycle

3–5 weeks

1  Laboratory animals

Select AE‑model‑sensitive animals, such as SJL/J, B10PL, PL/J mice, Lewy rats, guinea pigs, and domestic rabbits, among others.

1  Positive drug

Glucocorticoids, immunosuppressants, interferons, and other agents can suppress aberrant immune responses and mitigate central inflammation and neuronal damage.

1  Application areas

This model is primarily used for mechanistic studies of multiple sclerosis and other neuroimmune disorders, as well as for screening candidate drugs, evaluating drug efficacy, and validating therapeutic strategies.

Construction of an EAE animal model

They are mainly divided into active induction and passive induction methods.

Active induction method: An AE model is established by administering antigens in combination with adjuvants, with pertussis toxin used to enhance model induction. Throughout the experiment, animal body weight is continuously monitored, and neurological function scores are assessed according to established criteria. Subsequently, a range of assays can be performed, including lymphocyte proliferation assays, cell phenotyping, flow cytometry, as well as histopathological and immunohistochemical analyses of brain tissue, while also allowing verification of the organ-specific characteristics of the lesions.

Passive induction method: Antigen-specific T cells are isolated from the model animal and transferred into a healthy recipient to establish the disease model. These cells can be screened, labeled, and subjected to functional assays; subsequent observations monitor the onset of disease in the recipient, while cellular phenotyping of brain and spinal cord tissues is performed.

Model Evaluation

Clinical manifestations:

In mice, the disease was induced with an acute onset at 12 ± 3 days and reached a peak within 16 ± 2 days, with a variable duration; thereafter, recovery ensued, resulting in mild tail weakness or rigidity. The severity score of disease onset was 3.2 ± 0.6.

Neurological function score:

Body weight of the mice was measured starting from the day of autoimmune induction. Thirty-two days after immunization, neurological function scores were assessed using a double-blind method, with the following scoring criteria:

Level 0: No clinical manifestations;

Level 1: Lethargy and weakness in the tail.

Level 2: Abnormal gait, with weakness in both hind limbs.

Grade 3, bilateral hindlimb paralysis;

Grade 4: Paraplegia of both hind limbs accompanied by paresis or paralysis of one or both forelimbs.

Level 5: Near death or death. Relapse is defined as a clinical score higher than the previous episode after recovery from the initial onset, or a sustained score at the same level for more than 3 days.

Model features:

Sensitivity varies considerably among different animal strains. Rodent models of autoimmune encephalomyelitis closely recapitulate the clinical manifestations, pathology, immunological features, and biochemical alterations of human demyelinating diseases, making them widely applicable.