The most common form of dementia, Alzheimer’s disease, and a relatively rare hereditary form of dementia, frontotemporal dementia with parkinsonism-17, share a common pathology: Both are the result of an overaccumulation of tau proteins, which form tangled lesions in the brain’s neurons and eventually lead to the collapse of the brain cells responsible for memory
although mutations in the gene encoding tau have not been found in individuals with Alzheimer’s disease, they have been identified in individual with frontotemporal dementia, and are often used as models for studying Alzheimer’s disease
A new study finds that the Pin1 enzyme, previously shown to be of benefit in “detangling” tau in Alzheimer’s disease, actually has the contradictory effect in cases in which the tau has certain mutations
while increasing Pin1 in neurons effectively suppresses the disease development in cases of Alzheimer’s, it actually accelerates disease progression in the case of frontotemporal dementia