Silva and Ehninger studied mice bred with TSC and verified that the animals suffered from the same severe learning difficulties as human patients. Next, the UCLA team traced the source of the learning problems to biochemical changes sparking abnormal function of the hippocampus, a brain structure that plays a key role in memory.
"Memory is as much about discarding trivial details as it is about storing useful information," said Silva, a member of the UCLA Department of Psychology and UCLA Brain Research Institute. "Our findings suggest that mice with the mutation cannot distinguish between important and unimportant data. We suspect that their brains are filled with meaningless noise that interferes with learning."
"After only three days of treatment, the TSC mice learned as quickly as the healthy mice," said Ehninger. "The rapamycin corrected the biochemistry, reversed the learning deficits and restored normal hippocampal function, allowing the mice's brains to store memories properly."
In January, Silva presented his study at the National Institute of Neurological Disorders and Stroke meeting, where he was approached by Dr. Petrus de Vries, who studies TSC patients and leads rapamycin clinical trials at the University of Cambridge. After discussing their respective findings, the two researchers began collaborating on a clinical trial currently taking place at Cambridge to examine whether rapamycin can restore short-term memory in TSC patients.
"The United States spends roughly $90 billion a year on remedial programs to address learning disorders," noted Silva. "Our research offers hope to patients affected by tuberous sclerosis and to their families. The new findings suggest that rapamycin could provide therapeutic value in treating similar symptoms in people affected by the disorder."'
|Contact: Elaine Schmidt|
University of California - Los Angeles