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, especially when screening and testing drugs, as it may
produce diametrically opposite effects."
More information
The Alzheimer's Association has more about
current treatments for Alzheimer's.
