Irvine, Calif., May 31, 2007 -- A drug used to treat cancer has been shown to enhance long-term memory and strengthen neural connections in the brain, according to a new study by UC Irvine scientists.
In the study with mice, scientists found that histone deacetylase (HDAC) inhibitors currently used in clinical trials to attack cancerous tumors relaxes the protein structure that organizes and compacts genomic DNA, allowing for easier activation of genes involved in memory storage. This finding suggests that HDAC inhibitors could boost memory in humans and because of the way they work be therapeutic for people with Alzheimers and Huntingtons diseases and Rubenstein-Taybi syndrome.
We have demonstrated for the first time that HDAC inhibitors applied directly to the hippocampus enhance memory and synaptic plasticity in the brain, and we now know a molecular mechanism through which these enhancements occur, said Marcelo Wood, assistant professor in the Department of Neurobiology and Behavior at UCI and an author of the study.
This study appears June 6 in the Journal of Neuroscience.
A protein complex called chromatin causes genomic DNA to compress much like a telephone cord shortens as it coils. When chromatin loosens, genes associated with memory can activate more easily. Previous studies have shown that the protein CBP causes chromatin to relax, thus facilitating gene activation required for memory formation. The enzymes that reverse this process, or make the chromatin tighter, are known as HDACs. UCI scientists found in this study that HDAC inhibitors loosen chromatin and lead to stronger memory formation.
This is a fundamental aspect of molecular biology, and it is fascinating that it can impact memory, cancer and neurodegeneration and potentially other conditions such as drug addiction and other psychiatric disorders, said Wood, also a fellow of the UCI Center for the Neurobiology of Learning and Memory.