Finding could mean changing animal models used for future research
WEDNESDAY, April 23 (HealthDay News) -- An enzyme shown to help suppress development of Alzheimer's disease appears to hasten progress of a related but far less common type of dementia, according to a new study.
The surprising findings, published in the April 22 online issue of The Journal of Clinical Investigation, are significant, because individuals with frontotemporal dementia with parkinsonism-17 -- a relatively rare hereditary form of dementia -- are often used as models for studying Alzheimer's disease.
Alzheimer's disease and frontotemporal dementia each develop as a result of too many tau proteins accumulating and causing tangled lesions in the brain's neurons. These knotted nerve cells eventually choke off the brain cells responsible for memory.
However, individuals with frontotemporal dementia have mutations in the gene, known as P301L, encoding tau. These mutations have not been found in individuals with Alzheimer's.
Researchers found in mouse models and human cells that boosting levels of the prolyl isomerase (Pin1) enzyme, previously shown to aid in "detangling" tau in Alzheimer's disease, helps break down the tau proteins. However, the same experiments on mice with the genetic mutations in the tau that cause frontotemporal dementia resulted in increased and accelerated tau protein tangling.
"First, we have established a proof of concept that boosting Pin1 activity may offer a new idea for preventing or even treating the tau pathology and neurodegeneration in Alzheimer's disease," senior author Kun Ping Lu, a scientist in the Division of Hematology/Oncology at Beth Israel Deaconess Medical Center, said in a prepared statement. "And, second, given that no tau mutation is found in Alzheimer's patients, this research suggests that it would be prudent to not use P301L tau as an Alzheimer's disease model, espec
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