 We have published a model of Down syndrome using induced pluripotent stem cells. We find Down syndrome a very interesting phenomenon. First of all, it is the most common genetic cause of intellectual disability. Studying Down syndrome opens a lot of clues into many different diseases. This is because people with Down syndrome show a paradoxical relationship to many common diseases that they encounter in the general population. It should theoretically be prone to growing out of control, becoming a cancer cell. It should be prone to DNA damage. People with Down syndrome have a lot of related conditions. So they have, for example, obesity, they have hyperepidemia. So all these things should predispose them to a number of diseases such as type 2 diabetes, coronary disease, strokes and so on. On the other hand, they have a gene called the amyloid precursor protein on chromosome 21. And again, we see early Alzheimer's dementia in a fraction of people with Down syndrome, but the other fraction, a good half of them don't develop dementia, although they should. And it's these protective factors that are elusive that we still haven't fully understood. We hope that the model that we have published in this paper will be used in the future to dissect these mechanisms. So we've used the method of induced protein stem cells that allows us to take from any living person a donated cell that can be grown in a tissue culture and reprogrammed back to the stage similar to embryonic stem cells. It allows us to grow a patient's own brain cells from donated skin, blood or hair cells. There's a lot of variability which is introduced by comparing different clones from different people from different culture histories in the culture dish. So we approach this trying to generate as pure model as possible. We were fortunate to have consented surplus diagnostic material from such a person where skins were donated and the geneticist already found that there is mosaicism. We have established a system where we have the only genetic difference between the cell lines being trisomy 21 and the otherwise genetically identical. So we found that there were differences when we asked the embryonic-like stem cells, induced protein stem cells, to differentiate. And their ability to generate the optimal appropriate number of tissue-specific cells such as blood cells and brain cells. For example, we found that when they generate hematopoietic progenitors of blood cells, they tend to hyper-generate them. Whereas there is the opposite effect when they're trying to generate a neuro-progenitor cell. So that's one of the findings. The other finding we found was that the trisomic cells compared to the disomic produced a lot more of the amyloid protein which is the protein that is a key for the pathogenesis of Alzheimer's disease. We also found an interesting finding is that the brain cells developed from these induced protein stem cells in culture showed a lot more DNA damage and accelerated neuronal aging that we could monitor in a culture dish in the form of a foci that we detected in the nucleus of the neurons that were gamma 2AX, a foci that are indicator of DNA damage and a marker of aging. We hope to be able to use this model for understanding cellular aging as a general phenomenon in specific for Down syndrome genes that are present on chromosome 21. We could dissect the mechanisms of such cellular aging in neurons which could have wide implications for conditions such as mild cognitive impairment, Alzheimer's dementia and related conditions.