Alzheimer’s Disease (AD) Models

Wild Mouse 750
Wild Mouse 750
Human Xenograft Models
Cell Derived Xenograft Models
Autoimmune Disease Models
Systemic Lupus Erythematosus ModelsMultiple Sclerosis ModelsRheumatoid Arthritis ModelsPsoriasis ModelsInflammatory Bowel Disease ModelsAtopic Dermatitis Models Asthma Models
Metabolic Disease Mouse Models
Obesity ModelsDiabetes ModelsNon-alcoholic Steatohepatitis (NASH) ModelsHyperlipidemia ModelsOsteoporosis ModelsHyperuricemia Models
Humanized Immune System Models
huPBMC-NCGhuHSC-NCG-XhuHSC-NCG-hIL15huHSC-NCG
Organs or Tissue Humanized Mouse Models
Wild Mouse 765
Wild Mouse 765
Rare Disease Mouse Models
Progressive Muscular Dystrophy ModelsHemophilia A Models
Neurodegenerative Disease Mouse Models
Alzheimer’s Disease (AD) ModelsParkinson’s Disease (PD) ModelsHuntington's Disease (HD) ModelsAmyotrophic Lateral Sclerosis (ALS) ModelsTransthyretin Amyloidosis (ATTR) Models
Immuno-Oncology Mouse Models
Human Xenograft ModelsHumanized Immune Checkpoint ModelsHumanized Immune System ModelsSpontaneous Tumor Models

Alzheimer's disease is the most prevalent type of dementia. It is a progressive neurodegenerative disease that begins with memory loss. As the disease advances, symptoms can include problems with language, a decline in social and vocational functioning, executive dysfunction, personality changes, and behavioral issues.

There is no definitive explanation for the pathogenesis of Alzheimer's disease, and the mainstream ideas include the amyloid beta (Aβ) hypothesis and the tau hypothesis. Only six AD drugs have been approved to date, and these drugs can only delay disease progression or alleviate symptoms. A suitable animal model is a crucial research tool for Alzheimer's disease therapeutic development. GemPharmatech has developed two AD models that can be utilized for the screening and safety evaluation of Alzheimer's disease drugs.


Strain No.
 Strain Name Strain Type Description
T005625 FAD2T(APP/PS1) Transgenic The model randomly inserted two genes of Human mouse chimerism APP genes carrying humanized Aβ and Swedish mutations (K595N, M596L) and human PSEN1 (PSEN1-dE9, 9th exon deletion) into the genomes of C57BL/6 mice using murine prion promoters (Prnp) as promoters.The transgenic model mice exhibited a large number of Aβ plaque aggregation at 12 months of age. Astrocytes and microglia hyperplasia occur simultaneously in the cortex and hippocampus, and the mice developed spatial memory impairment.
T058996 FAD4T-hTREM2 Transgenic The TREM2 humanized FAD4T-hTREM2 mouse model was constructed based on the FAD4T background, which can be used to evaluate the efficacy of monoclonal antibodies or small molecule drugs. It can also be used to explore the function and regulatory mechanism of TREM2 signaling central hub to explore the immunotherapy for AD disease.
T056008 B6-hTREM2 KI GemPharmatech has developed humanized mouse models targeting the TREM2 signaling pathway on B6 backgrounds, which can be used for efficacy evaluation of monoclonal antibodies or small molecule drugs and to explore immunotherapy against myeloid-mediated diseases by investigating the function and regulatory mechanisms of the central hub of TREM2 signaling.
T053302 FAD4T Transgenic Human APP gene with Swedish and Indiana mutations and human PSEN1 gene with M146V and L286V mutations were inserted into the mouse genome. Aβ deposition was detected in FAD4T mice at 1.5 months of age, and increased gradually with age. The activation of astrocytes and microglia in FAD4T mice can be detected at 2.5 months. FAD4T mice show spatial learning and cognitive deficits at 8 months of age. This model is applicable to the study of Alzheimer's disease and potential therapeutics for AD.
T049751 FAD3T(APP/PS1/Tau) Transgenic GemPharmatech established a novel model named FAD3T(APP/PS1/Tau), which carrying the human APP protein with Swedish mutation, human PSEN1 protein with M146V mutation and MAPT protein with P301L mutation. In 4-month-old FAD3T(APP/PS1/Tau) mice, Aβ plaque deposition was detected in the cortex and hippocampus, while tau protein and phosphorylated tau protein showed significant increases. In addition, FAD3T(APP/PS1/Tau) mice developed deficiency in spatial learning and memory at 6 months of age. This model can simulate the pathological characteristics and neurobehavioral phenotype of AD.