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Some researchers at Johns Hopkins gave an anti-cancer compound to adolescent mice with a rodent version of schizophrenia.
The compound, called FRAX486, seemed to reverse rodent behaviors related to schizophrenia and surprisingly, some of their disrupted brain cell function was restored.
The FRAX486 compound appears to stop a neurological pruning process that goes on in a schizophrenic brain. Pruning refers to the destruction of significant neural connections, disrupting brain communication.
“By using this compound to block excess pruning in adolescent mice, we also normalized the behavior deficit,” said study leader Akira Sawa, M.D., Ph.D. “That we could intervene in adolescence and still make a difference in restoring brain function in these mice is intriguing.”
Most human symptoms of schizophrenia first occur in late adolescence or early adulthood. So, the scientists believe their findings with the teenage mice holds promise in developing more effective therapies for humans with schizophrenia.
There is a gene called Disrupted-in-Schizophrenia 1 (DISC1). This gene’s protein seems to be responsible for the health of cerebral cortex neurons used for information processing and “higher-order” functions.
In mice, a problem with DISC1 alters the development of two more proteins necessary for the proper growth of neuronal spines. The spines help one neuron talk to another. When the proteins are out of balance, the spines get pruned.
By applying FRAX486, the rodents’ neuronal spines were protected from demise and missing spines were restored. The mice also demonstrated less schizophrenia associated behavior.
What researchers need to determine now is whether the same disruptive protein cascade occurs in humans as in mice.
Two promising details about FRAX486 are that only a small amount was needed to protect the rodent brain cells, and the mice experienced no nasty side effects from the compound. Furthermore, FRAX486 does double duty as both a healer and protector.
“Drugs aimed at treating a disease should be able to reverse an already existing defect as well as block future damage,” says Sawa. “This compound has the potential to do both.”
Now, for all this promising data related to improving schizophrenia treatment, a note of thanks to the intrepid research mice who likely did not volunteer to have their DISC1 gene tampered with.
Source: Hopkins Medicine
Photo credit: Christopher Parente
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