Hopkins study exposes potential schizophrenia drug target
Johns Hopkins researchers have tied together two culprits behind schizophrenia and believe that their discovery could pave the way to new drugs that combat cognitive impairment caused by the mental disorder.
The researchers studied the mutated DISC1 gene, a major risk factor for schizophrenia, in brain cells called astrocytes that play a key role in communication among neurons. Astrocytes, a type of glia cell, secrete the neurotransmitter D-serine, which aids in glutamate transmission. Decreased glutamate transmission has also been linked with schizophrenia.
Confirmed in mouse experiments, Drs. Mikhail Pletnikov and Solomon Snyder's research concluded that the DISC1 gene directly impacts output of the D-serine neurotransmitter via binding to the enzyme known as serine racemase. Mutated DISC1 won't bind correctly with the enzyme, causing the key enzyme to wither and leading to low levels of the neurotransmitter. They believe that a drug that stabilizes the connection between mutated DISC1 and the enzyme could improve the thought processes in schizophrenics.
Other researchers have already hit the clinic with treatments to ratchet up D-serine levels in patients with schizophrenia. By targeting the mutated DISC1-enzyme connection, drugs could potentially boost glutamate transmission, which is believed to be a factor in schizophrenia and a range of other mental impairments.
"Abnormal glutamate transmission is believed to be present in patients with bipolar disorder, major depression and possibly anxiety disorders, so our findings could apply to other psychiatric diseases," Pletnikov says in a release.
- here's the press release