An enzyme that produces a toxic protein involved in Alzheimer disease is also important for myelination or insulation of nerve cell axons, according to a study in the December 2006 issue of Nature Neuroscience. These results suggest that targeting this enzyme (BACE1) as a treatment for Alzheimer disease may produce significant adverse side effects.
Most nerve cell axons are wrapped with a layer of myelin, which acts like an insulator of electrical wires to allow nerve impulses to travel more quickly to their destination. Riqiang Yan and colleagues studied mice with a deletion of the BACE1 gene to determine the effects of eliminating this enzyme. The thickness of the myelin sheath in these mice was reduced along axons throughout the brain and spinal cord. These effects were visible as early as 15 days following birth and lasted into adulthood. The authors show that under normal conditions BACE1 exerts its effect by activating neuregulin, a known participant in the initiation of myelination.
Behavioral testing also revealed that these mice exhibited lower pain thresholds and decreased grip strength - typical signs of demyelination. Although inhibition of BACE1 may be a viable candidate for reducing the conversion of amyloid precursor protein into the plaques deposits seen in Alzheimer disease, these results suggest that as a therapeutic technique, it should be approached with caution.
Riqiang Yan (Cleveland Clinic, Cleveland, Ohio, USA)
Abstract available online.
(C) Nature Neuroscience press release.
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