Researchers at the Gladstone Institute of Neurological Disease recently published their research showing that removing a protein-regulating enzyme from mice suppressed Alzheimer’s symptoms in an animal model of the disease.
The researchers created genetically modified mice that expressed different levels of an enzyme known as Fyn. Fyn regulates the activities of many proteins. With Alzheimer’s disease, amyloid proteins accumulate in the brain and destroy synapses. In mice genetically engineered to completely block Fyn, however, the amyloid proteins were unable to damage the synapses and the mice lived much longer than typical mice used in the Alzheimer’s disease model.
Lead researcher Jeannie Chin said of the findings,
Our results suggest that Fyn lays a key role in Alzheimer’s-related synaptic impairments, and that it can worsen the toxicity of amyloid proteins. We are excited about the possibility that pharmacological modulation of Fyn might be of therapeutic benefit in this disease.
As Fyn plays a key role in a number of neurological processes, it is unlikely that it could be completely suppressed in human beings without severe side effects. The researchers plan to conduct further research to quantify what sort of benefit, if any, mice in the Alzheimer’s model receive from partial suppression of the enzyme.
Source:
Alzheimer’s pathology reduces, longevity improved in mouse model, Gladstone study shows. Press Release, University of California – San Francisco, May 19, 2004.