In previous studies, Zakharenko’s group found that abnormal nerve cell communication and cognitive dysfunction was associated with elevated levels of a protein that regulates calcium in certain nerve cells known as Serca2. These abnormalities are only detectable with age in mice with the 22q11 deletion.
In the current study, the researchers identified the gene Dgcr8 as the source of the changes. It produces molecules called microRNAs that normally keep Serca2 in check. Without them, the protein becomes elevated. By adding these molecules back into the hippocampus of animals with the 22q11 deletion, the researchers were able to reduce elevated Serca2 levels and reduce the cellular deficits associated with this genetic defect.To assess whether the findings from these genetic mouse studies might translate to schizophrenia, the authors analyzed post-mortem brain tissue from people with schizophrenia. The researchers discovered that Serca2 was elevated even in patients with schizophrenia who did not have the 22q11 deletion.
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