Scientists from Mount Sinai have learned how mutated tau proteins cause deterioration in neurons associated with FTD.

Alison M. Goate, DPhil, director of the Loeb Center for Alzheimer’s Disease at Mount Sinai, said in a press release that researchers there “identified several very early transcriptomic and proteomic changes that lead to the formation of tau pathology and neuronal death.

“Our goal is to help researchers develop novel treatments against frontotemporal dementias and prevent the suffering experienced by patients and their families,” she added.

The study — published in Cell and partially funded by AFTD — involved scientists recreating the brain damage caused in FTD disorders. The process included growing cerebral organoids in petri dishes made from induced pluripotent stem cells (iPSCs). Researchers examined thousands of 3D cerebral organoids, which mimicked the early growth and development of the cerebral cortex.

Sally Temple, PhD, scientific director of the Neural Stem Cell Institute and a senior author of the study, said in the press release that the iPSCs allow researchers to study each participant’s personalized disease in a petri dish.

“By combining iPSC-organoid technology with high-throughput, single cell gene activity analysis, we were able to get a better look at what might be going on in a patient’s brain at early stages of disease development, even before symptoms emerge,” Temple said.

Read the full Mount Sinai press release here.