"We are seeing what appears to be the same sort of thing happening as a result of abnormal influences," said Greenough, who holds a Swanlund Endowed Chair at the University of Illinois at Urbana-Champaign. "It appears that in both Fragile X and schizophrenia patients, abnormalities of the plasticity processes are occurring, or maybe some other genetic mechanism is driving the molding of the brain in the wrong directions."
Fragile X syndrome is an inherited condition and the leading cause of mental retardation in males. Schizophrenia is a severe emotional disorder involving misperceptions of reality, delusions and hallucinations.
Greenough is studying both conditions. He and Illinois colleague I.J. Weiler were the first to report that the Fragile X protein that is missing in the syndrome is synthesized at synapses. Synapses are the connections through which nerve cells communicate. Brain exams of deceased Fragile X sufferers revealed that nerve cells in the cerebral cortex had an overabundance of long, malformed dendritic spines the receiving part of the synapse.
Earlier this month in the journal Neuron (Feb. 6), Greenough's team, in collaboration with the University of Pennsylvania School of Medicine, reported the presence of the glucocorticoid receptor among numerous molecules found in messenger RNA of the Fragile X protein. The receptor is necessary for the regulation of circulating levels of adrenal corticosteroids. Closer evaluation showed the receptor is in cells and dendrites of the brains of normal mice but absent from the dendrites of mice modified to not produce the Fragile X protein.