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Dementia is an umbrella term used to describe various cognitive degenerative diseases. A common form of dementia is Alzheimer’s disease. A relatively rare hereditary form of dementia is frontotemporal dementia (FTD) with parkinsonism-17. Both of these forms of dementia share a common pathology–an over accumulation of tau proteins, which form tangled lesions in the brain’s neurons which eventually lead to the collapse of the brain cells responsible for memory.

Kun Ping Lu, MD, PhD, scientist, Division of Hematology/Oncology, Beth Israel Deaconess Medical Center (BIDMC) reports that the enzyme Pin1, which has been shown to ‘detangle’ the tau protein in Alzheimer’s, may actually have the reverse effect and accelerate dementia in the FTD form of the disease.

Researchers found that when Pin1 was present the tau proteins readily degraded. When the Pin1 enzyme was removed the tau proteins failed to break down.

When the experiment was performed on mice that were genetically engineered to model either the over-expressed Pin1 enzyme or model Alzheimer’s disease researchers were astonished at the result. Not only did the exact same Pin1 over-expression not suppress tau stability, it actually increased the tau protein’s neurodegenerative activity.

Researchers suggest their findings show that they established proof that Pin1 activity may offer a new approach for treatment of Alzheimer’s disease. Also, Alzheimer’s researchers should avoid using mice models that include P301L tau along with Alzheimer’s disease model.

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