Alzheimer's Disease Model
Alzheimer's disease is the leading cause of dementia, accounting for about two-thirds of all dementia cases. This common neurodegenerative disease usually results in severe memory impairment. The lack of effective cures makes it important to increase the development and characterization of relevant animal models to facilitate disease mechanisms and drug development research.
Our company' scientific team has extensive expertise in providing clients with scientifically sound and reliable animal models of Alzheimer's disease to facilitate their research in related diseases, based on scientific methodological techniques and evaluation tools.
Introduction of Alzheimer's Disease
Alzheimer's disease is a neurodegenerative disorder that often occurs in old age, with typical cognitive impairment and behavioral impairment as the main clinical manifestations. The pathology is mainly characterized by the formation of neuronal fiber tangles from abnormally phosphorylated Tua protein in brain cells and the formation of age spots from extracellular interstitial beta amyloid deposits. The specific etiology and pathogenesis of Alzheimer's disease are still unclear, and effective early interventions and treatments are lacking. Therefore, basic research to explore the pathogenesis of AD is important for the prevention and treatment of the disease.
Application of Mouse Models in Alzheimer's Disease
Mouse models are one of the most important research tools in the search for new therapies for Alzheimer's disease.
- Mice are highly phylogenetically protected from humans in the structure and function of hippocampal and internal olfactory cortex circuits that mediate episodic memory and are vulnerable in Alzheimer's disease.
- Mice have a similar number of genes and a considerable amount of chromosomal homology to humans.
- The mouse model provides a sufficiently simplified system to facilitate experimental manipulation.
- Mouse models of Alzheimer's disease are useful as a tool for target identification and validation.
Fig. 1 Schematic diagram of the main animal models of Alzheimer's disease. (Drummond, 2017)
The Alzheimer's Diseases Models We Provide
Animal models of Alzheimer's disease are essential to better understand the pathogenesis and to assess the potential of new therapeutic approaches.
The neuroscience experts at Our company, fully understand the strengths and limitations of each animal model of Alzheimer's disease. We offer our clients a multi-strategy approach to modeling. We provide models that well simulate not only the major pathological features and neurobiochemical and other changes in AD, but also the behavioral changes in AD.
The Alzheimer's disease models we offered include, but are not limited to the following.
- Aging animal models
| Aging Animal Models | Description |
|---|---|
| Natural aging model | Animal models of AD obtained by natural aging of the animals themselves, including aged rats and mice. |
| Senescence accelerated mouse model (SAM) | Obtained by inbred extended generation culture of AKR/J natural mutant mice. |
- Chemical injury animal models
The model was established mainly by injecting specific substances into the brain, subcutaneously or intraperitoneally of model rats.
| Chemical Injury Animal Models | Description |
|---|---|
| Aβ induction model | Multiple injections of Aβ fragments in the CA1 region of the hippocampus or lateral ventricles induce Aβ deposition, formation of SP. |
| Scopolamine (SCOP) induction model | SCOP is a cholinergic antagonist, and intraperitoneal injection of SCOP causes dysfunction of the cholinergic system in model animals, resulting in cognitive decline. |
| IBO induction model | AD model induced by intracerebral bilateral IBO injection. |
| STZ induction model | STZ is injected into the lateral ventricle of the animal, which destroys the normal metabolism of sugar and energy in the brain. |
| D-galactose model | Subcutaneous continuous injection of D-gal can establish a subacute aging animal model. |
| OKA induction model | Injection of OKA at different sites in rat brain induces hyperphosphorylation of Tau protein. |
- Transgenic animal models
Transgenic animal models are the most widely used models in AD research. Our company offers transgenic animal models including but not limited to the following.
| Transgenic Animal Models | ||
|---|---|---|
| PDAPP mouse model | Tg2576 mouse model | APP23 mouse model |
| TgCRND8 mouse model | APP/PS-1 double transgenic model | APP/PS1/Tau triple transgenic model |
| 5XFAD transgenic model | ||
Evaluation Methods for The Alzheimer's Disease Models
Behavioral researches are very important indicators used to evaluate neurodegenerative diseases, including AD, and can be used to assess the degree of similarity of models to human diseases. Our company uses a variety of advanced experimental equipment and methods for testing the behavior of AD models, and we offer behavioral assessment methods including, but not limited to the following.
| Behavior | Testing Methods | ||
|---|---|---|---|
| Cognitive | Morris water maze test | Barnes maze test | Radial arm maze test |
| Y-maze test | T-maze test | 5-CSRTT test | |
| Touch screen test | |||
| Anxiety | Elevated plus maze test | Open field test | Light-dark box test |
| Sucrose preference test | Forced swimming test | Tail suspension test | |
| Social | Three-chamber test | Social interactions test | |
| Motor | Beam test | Rotarod test | General locomotor test |
| Gait analysis test | Pole test | Rearing cylinder test | |
| Ladder rung walking test | |||
Our company is committed to combining our specialized experimental platform and extensive scientific knowledge to jointly provide effective research models for the development of the field of neuroscience. If you are interested, please contact us and describe your specific research, and we will be happy to assist you.
References
- Drummond, E.; et al. Alzheimer's disease: experimental models and reality. Acta neuropathologica. 2017, 133(2): 155-175.
- Hall A, M.; et al. Mouse models of Alzheimer's disease. Brain research bulletin. 2012, 88(1): 3-12.