>90% of documented AD cases are sporadic in nature. However, almost all availale AD animal models and cell models are created based on mutations linked to familial AD. Without these mutations, the experimental models will not be able to generate high levels of amyloid-beta to induce cellular and tissues changes mimicking features in AD. The neuropathology of familial and sporadic AD are rather similar. The major differences are earlier onset in familial cases.
The article highlighed in the SDL3 only document using iPS on familial AD experimental model. However, there are some review papers discussing the possible use of iPS on sporadic AD. You can evaluate these thoughts to strength your arguments.
The objective of this SDL is to test your critlcal thinking and analysis skills, rather than "synthesizing" available information into desired format.