sinapsisA new drug developed by researchers at Yale School of Medicine could help reverse cognitive impairments caused by Alzheimer’s disease. The results of this work were published in the journal PLoS Biology.

The compound, TC-2153, inhibits the negative effects of a protein called STtriatal-Enriched tyrosine Phosphatase (STEP), which is key to regulating learning and memory. “Decreasing STEP levels reversed the effects of Alzheimer’s disease in mice,” said lead author Dr. Paul Lombroso, professor in the Yale Child Study Center and in the Departments of Neurobiology and Psychiatry at Yale School of Medicine.

The team of researchers led by Lombroso studied thousands of small molecules, searching for those that would inhibit the activity of STEP. Once identified, the researchers tested compounds that inhibit STEP in brain cells to examine their effectiveness.

According with the researchers, high levels of STEP proteins keep synapses in the brain from strengthening. Synaptic strengthening is a process that is required for people to turn short-term memories into long-term memories. When STEP is elevated in the brain, it depletes receptors from synaptic sites, and inactivates other proteins that are necessary for proper cognitive function. This disruption can result in Alzheimer’s disease or a number of neuropsychiatric and neurodegenerative disorders.

Lombroso said: “A single dose of the drug results in improved cognitive function in mice. Animals treated with TC compound were indistinguishable from a control group in several cognitive tasks.”

The team is currently testing the TC compound in other animals with cognitive defects, including rats and non-human primates. Lombroso, who is positive about the potential of his study said: “These studies will determine whether the compound can improve cognitive deficits in other animal models […] Successful results will bring us a step closer to testing a drug that improves cognition in humans.”