Frontotemporal dementia (FTD) refers to a spectrum of clinical diseases that may have several different underlying pathologies. Frontotemporal dementia can be sporadic or associated with mutations in the MAPT (microtubule-associated protein tau) and progranulin genes, and C9ORF72 repeat expansions.
These genetic mutations can lead to accumulation of TDP43 protein or tangles of MAPT (tau) protein. Currently, there are no approved treatments or reliable biomarkers for frontotemporal dementia. There is a need for in vitro human cell models for frontotemporal dementia and Alzheimer’s disease that can be used to accelerate research and assist in the development of new drugs to treat these disorders.
Human iPSCs from Frontotemporal Dementia patients
Fibroblasts from patients clinically diagnosed with Frontotemporal Dementia were reprogrammed to iPSCs using Sendai reprogramming. These FTD lines are available with mutations in MAPT genes, from Paget’s Disease patients, and patients exhibiting FTD and ALS symptoms.
Fibroblasts (43 Yr Female)
Fibroblasts (42 Yr Male)