Alzheimer’s Disease (AD)

Alzheimer's disease (AD) is a progressive, irreversible neurodegenerative disorder characterized by memory impairment, cognitive decline, and executive dysfunction often accompanied by language disorders, motor impairment, personality changes, and neuropsychiatric symptoms. GemPharmatech has developed several AD models for the screening and safety evaluation of Alzheimer's disease drugs.

50+
Neurological Disease Mouse Models
500+
Studies Completed
10+
IND-Enabling Studies

Advantages

Our Advantages

Industry-leading capabilities for Alzheimer’s Disease Research

Clinically Relevant Models

Our AD models closely mimic human disease progression, including amyloid-beta (Aβ) plaque deposition and Tau protein tangle formation — the two core pathological hallmarks of Alzheimer's disease.

Comprehensive Assessment

Multi-parameter evaluation including behavioral testing (spatial learning and memory), pathological staining (Aβ, GFAP, IBA1), and biochemical analysis.

Customizable Study Design

Flexible protocols for acute and chronic AD studies, with options for pharmacological induction and humanized model combinations. Models support evaluation of monoclonal antibodies, small molecule drugs, and BBB transport strategies.

Model Library

Case Studies

Case Studies & Validation Data

Trontinemab / Lecanemab Therapeutic Efficacy

Therapeutic Efficacy of Trontinemab / Lecanemab in FAD4T-hTFRC Mouse Model

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Therapeutic Efficacy of Trontinemab / Lecanemab in FAD4T-hTFRC Mouse Model

In FAD4T-hTFRC mice, treatment was initiated at 2.5 months of age. Following 14 weeks of dosing, brain tissues were harvested and subjected to staining for Aβ, GFAP, and IBA1. The results demonstrated that Trontinemab achieved better clearance of cerebral Aβ plaques compared to Lecanemab.

Trontinemab Therapeutic Efficacy

Therapeutic Efficacy of Trontinemab in FAD3T-hTFRC Mouse Model

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Therapeutic Efficacy of Trontinemab in FAD3T-hTFRC Mouse Model

In FAD3T-hTFRC mice, treatment was initiated at 1 month of age. Following 8 weeks of Trontinemab treatment, the protein expression levels of Aβ40 and Aβ42 in the cortex and hippocampus were significantly reduced.