A recognized hallmark of Alzheimer's disease is TAU protein malfunction, which leads to self-protein aggregation and, eventually, neurodegeneration. There has been an increased focus on aggregation-prone proteins, and on the role of non-neuronal cell populations such as microglia and astrocytes. However, no disease-modifying therapy has been found to date.
The use of models that closely mimic Alzheimer's pathophysiology in vitro can help diminish the translational gap and advance therapeutic candidates through your pipeline faster. Human iPSC-derived models can help understand Alzheimer's etiology and predict the efficacy of new therapeutic candidates with higher confidence.
This case study describes how Ncardia successfully developed an Alzheimer’s disease model, using insoluble fractions of brain homogenates to mimic Alzheimer's disease etiology.
Download the case study and discover the benefits:
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Derived from patient material to closely mimic human pathophysiology
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Adaptable to display a range of phenotypes, depending on your needs
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Characterization assays and high-throughput screening readily available