Thursday, November 16, 2006
CLEVELAND, Nov. 16 (UPI) -- U.S. researchers have determined an enzyme that produces a toxic protein involved in
Alzheimer's disease is also important for nerve cell myelination.
The finding by Riqiang Yan and colleagues at the Cleveland Clinic suggests targeting the BACE1 enzyme as an Alzheimer disease treatment might produce significant adverse side effects.
Most nerve cell axons are wrapped with a layer of myelin, which acts as an insulator to allow nerve impulses to travel more quickly to their destination. Riqiang Yan and colleagues studied mice with a deletion of the BACE1 gene.
The researchers found the thickness of the myelin sheath in the mice was reduced along axons throughout the brain and spinal cord. Those effects were visible as early as 15 days following birth and lasted into adulthood.
The mice also exhibited lower pain thresholds and decreased grip strength -- both typical signs of demyelination.
The researchers concluded that although inhibition of BACE1 may reduce the conversion of amyloid precursor protein into the plaques deposits seen in Alzheimer disease, the study's results suggest that as a therapeutic technique, it should be approached with caution.
The research is presented in the December issue of Nature Neuroscience.
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