Cool! Has anything similar been attempted in tumor tissue, given the many claims of microbes in tumors? Especially tumors not in contact with the exterior.
J.J. and D.H. led the research. J.J., R.E., A. Pritzel, M.F., O.R., R.B., A. Potapenko, S.A.A.K., B.R.-P., J.A., M.P., T. Berghammer and O.V. developed the neural network architecture and training. T.G., A.Ž., K.T., R.B., A.B., R.E., A.J.B., A.C., S.N., R.J., D.R., M.Z. and S.B. developed the data, analytics and inference systems. D.H., K.K., P.K., C.M. and E.C. managed the research. T.G. led the technical platform. P.K., A.W.S., K.K., O.V., D.S., S.P. and T. Back contributed technical advice and ideas. M.S. created the BFD genomics database and provided technical assistance on HHBlits. D.H., R.E., A.W.S. and K.K. conceived the AlphaFold project. J.J., R.E. and A.W.S. conceived the end-to-end approach. J.J., A. Pritzel, O.R., A. Potapenko, R.E., M.F., T.G., K.T., C.M. and D.H. wrote the paper.”
These cells won’t divide because they will fail to replicate their DNA due to the lack of thymidine. The use case is cell therapies, where you give the patient cells grown in the lab but you don’t want those cells to potentially divide and cause cancer. For example, CAR T therapy to treat cancer, or dopaminergic neuron replacement therapy for Parkinson’s disease.
TERT activation is one of the most common alterations causing cancer. In fact, the whole point of the normally very low TERT expression in somatic cells is likely to be cancer prevention. It’s the mechanism behind the Hayflick limit, which puts a bound on the max number of divisions a cell can go through, via telomere shortening. Without such a limit, you get cancer. I highly doubt it will make you live longer.
Freezing and thawing organoids is not new, it’s fairly routine. The frozen piece of brain from an epilepsy patient doesn’t retain ”normal function”. There is no evidence in the paper that it integrates into neuronal circuits (this was not even tested), or supports anything like normal neuronal firing. The cells are alive, yes, and likely highly abnormally perturbed.
No that would be amazing. But we don’t have the technology to map all the connections in large mammalian brains. It was done in the fruitfly just this year: https://www.science.org/doi/10.1126/science.add9330
None, that was done 100 years ago, e.g. by Ramon y Cajal (Nobel prize 1906). But microscopic detail does not give molecular detail. What these current studies add is data on gene expression (mRNA molecules), chromatin accessibility (related to gene regulation), electrophysiology (in some cases), etc. We need such detail to connect disease genes inferred from genetics to specific brain cell types, for example.
The NIH BRAIN initiative is working on the next generation of that, covering more timepoints and better spatial data.