The key to reversing the progression of Alzheimer’s disease may be inhibiting a certain protein in the brain, according to Yale University researchers.  A study published in Proceedings of the National Academy of Science pointed to high levels of striatal-enriched tyrosine phosphatase (STEP) as a possible factor causing Alzheimer’s.

Earlier studies have shown high activity levels of STEP in people with Alzheimer’s.  Based on that, the Yale researchers tested two sets of mice that were genetically engineered to have Alzheimer’s.  One set, however, was engineered to have reduced STEP protein levels.  The result is that the mice with reduced STEP levels ultimately completed mazes in the same amount of time as mice who did not have Alzheimer’s. “The importance of that study is that it suggested that reducing STEP levels genetically reduces” Alzheimer’s effects, said Paul Lombroso, senior author.

According to Lombroso, an overabundance of STEP damages certain brain neurons.  The researchers learned that the protein removes glutamate receptors on the neuron’s surface, which are critical to creating long-term memories.  “This suggests that a too-high level of STEP, by removing glutamate receptors, is stripping away the ability to memorize and learn,” Lombroso, a professor at the Yale Child Study Center and at the Yale School of Medicine, said.  STEP has also been found to play a similar role in schizophrenia and fragile x, a type of mental retardation.

Chris Van Dyck, director of Yale’s Alzheimer’s Disease Research Unit, thinks the study is “exciting research.  We know that with Alzheimer’s disease, synaptic function is key to cognitive deficit.  This is an important paper that attempts to explain that,” he said, adding that more research is required “because mice are not people and these Alzheimer’s mouse models are limited.”