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A team at the Institute of Science Tokyo has developed a drug candidate that may extend the period during which motor functions lost due to a stroke can be recovered, currently limited to about two months, by suppressing a type of protein.
People who lose the ability to speak or to move their hands or feet after the death of nerve cells in the brain due to a cerebral infarction can regain these functions to a certain extent through rehabilitation.
This recovery is possible because surviving nerve cells repair the neuron networks, with microglia — cells in charge of brain immunity — helping the restoration process by secreting a protein called insulin-like growth factor 1 (IGF1).
Takashi Shichita, a professor at the institute's Medical Research Laboratory, and other members of the team conducted research on mice involving genetic manipulation. The team discovered that microglia stopped secreting IGF1 after a while following a stroke due to the function of another protein, ZFP384. The same mechanism was confirmed in the brains of dead stroke patients.
The team developed the drug candidate to block the production of ZFP384. After injecting the drug into mice, the team found that microglia continued to secrete IGF1 and helped maintain the recovery of brain functions.
The drug is a type of antisense oligonucleotide (ASO) that binds to messenger RNA (mRNA) from the ZFP384 gene and helps break down the protein. ASO therapy is starting to be used to treat intractable neurological disorders.
Shichita said that the drug candidate still needs to be tweaked to further enhance its efficacy for human use.
“We will work hard toward delivering the drug to patients in 10 to 20 years,” Shichita said.
The team's findings were published on the online edition of British scientific journal Nature on Wednesday.
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