การศึกษาการตอบสนองระดับโมเลกุลและระดับเซลล์ภายหลังการเหนี่ยวนำให้เกิดอะไมลอยด์ด้วยโมเลกุลขนาดเล็กในเซลล์ประสาทเพาะเลี้ยงแบบ3 มิติเพื่ออธิบายการเปลี่ยนแปลงในระยะเริ่มต้นของโรคอัลไซเมอร์

The aggregation of amyloid beta 42 predominately presents in the amyloid plaque of Alzheimer's brain. It is believed to play a central role in the pathogenesis of Alzheimer's disease. Intriguingly, amyloid beta 42 plays a role in both physiological and pathological functions depending on its conformation. In this study, the small molecule-induced amyloidosis will be generated in the human neuronal cell line. The small molecule; Aftin acts on the beta and gamma-secretase enzymes which induces the overproduction of amyloid beta 42 but no other amyloid beta isoforms. This results in several pathological features as presence in Alzheimer’s brain. By utilizing this disease modeling, we propose to identify the transcriptomes and cellular responses following amyloidogenic processing in vitro which distinguish between physiological and pathological roles of amyloid beta 42. This study will provide a better understanding of the pathogenesis of amyloidogenic pathway and reveal the molecular targets to delay Alzheimer's disease progression. Also, this cell culture model can be used as a screening prototype to identify the anti-amyloidosis potential from herbal extracts, which subsequently use to prevent Alzheimer’s disease.