Researchers from the Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School have generated induced pluripotent stem cell (iPSC) lines from patients harboring the London familial AD (fAD) amyloid precursor protein (APP) mutation (V717I). They found that during differentiation of the iPSC towards neuronal fate, APP expression and levels of Aβ increase dramatically. In addition, an increase in levels of total and phosphorylated Tau was also observed in neurons with the APPV717I mutation. Treating the neurons early in culture with Aβ-specific antibodies, reversed the phenotype of increased total Tau levels.
In this paper, the researchers generated iPS cells from sporadic and familial AD patients and differentiated them into neural cells. Aβ oligomers accumulated in iPSC-derived neurons and astrocytes in cells from patients with a familial amyloid precursor protein (APP)-E693Δ mutation and sporadic AD, leading to endoplasmic reticulum (ER) and oxidative stress. The researchers then analysed the oligomers and found they were not proteolytically resistant, and docosahexaenoic acid (DHA) treatment alleviated the stress responses in the AD neural cells.
This is a great example for the potential of patient-derived iPS cells to serve as a disease model. This cell model enables to study cellular mechanisms that are involved in the disease, and also serve as a screening test for various molecules or chemicals with therapeutic potential.
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