Alzheimer’s Disease (AD) Models

Autoimmune Disease Models
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Wild Mouse 750
Wild Mouse 750
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huPBMC-NCGhuHSC-NCG-XhuHSC-NCG-hIL15huHSC-NCG
Organs or Tissue Humanized Mouse Models
Wild Mouse 765
Wild Mouse 765

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by an insidious onset and progressive development. The primary clinical features of the disease include progressive memory impairment, cognitive decline, executive dysfunction, as well as accompanying language disorders, motor function impairment, personality changes, and neuropsychiatric symptoms.

Pathological studies indicate that AD progression is closely linked to the accumulation of amyloid-beta (Aβ) protein fragments and Tau protein tangles (paired helical filaments). There is currently no treatment that can fully prevents or reverses AD progression, underscoring the critical need for new and effective treatments. In this context, the establishment of animal models that can accurately simulate the pathological features and clinical manifestations of AD has become an indispensable research tool in the development of new AD drugs.

GemPharmatech has developed three AD models that can be utilized for the screening and safety evaluation of Alzheimer's disease treatments.

Strain No.
 Strain Name Strain Type Description
T053302 FAD4T Transgenic In this model, Aβ can be detected as early as two months of age, gliosis in the cortex and hippocampus can be observed from two months of age, and female mice exhibit spatial learning and memory deficits at eight months of age.
T049751 FAD3T(APP/PS1/Tau) Transgenic In this model, Aβ plaque deposition appears in the cortex and hippocampus at 2 months of age, and elevated phosphorylated Tau levels are detectable in one-month-old mice, with levels increasing over time. Additionally, female mice exhibit spatial learning and memory deficits at three months of age, with similar deficits appearing in males at four months.
T005625 FAD2T(APP/PS1) Transgenic In this model, Aβ plaque deposition becomes evident in the cortex and hippocampus by four months of age. By six months, the mice exhibit gliosis, and by eight months, they show significant deficits in spatial learning and memory.