Scientists at Weill Cornell Medicine have created a human neuron model that accurately mimics the spread of tau protein aggregates in the brain, which is responsible for cognitive decline in Alzheimer’s disease and frontotemporal dementia. This model has led to the identification of potential therapeutic targets to prevent tau spread, a significant advancement in Alzheimer’s disease research. By using CRISPR technology to modify the genomes of human stem cells, the researchers were able to simulate tau spread in neurons within weeks, a process that typically takes decades in aging brains. The discovery of the UFMylation cascade as a potential target for inhibiting tau spread in neurons is a promising development in the quest to develop new treatments for Alzheimer’s disease.
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Human neuron model identifies potential therapeutic targets for Alzheimer’s disease
