A new study conducted by Institute researchers, with colleagues in Italy, shows that decreased expression of two specific genes in isolation improves cognition but, paradoxically, reduced expression of both genes at the same time has the opposite effect.
AstraZenecatoday announced that it has entered into a two-year research collaboration with the Lieber Institute for Brain Development(LIBD) to use genetics and stem cell biology to discover new drugs for neuropsychiatric and neurodevelopmental disorders such as autism and schizophrenia.
The Lieber Institute emphasizes flexibility, collaboration, physical contiguity of interdisciplinary scientists, decision making based on scientific priority and opportunity, all in the context of a mission.
With a unique, multi-faceted approach, a Lieber research team has quantified the effect of previously unidentified anomalies in genetic expression that determine how the human brain develops from its earliest stages.
Lieber researchers have discovered that variability in a gene for the dopamine transporter (DAT)—a protein that directly controls the availability of the neurotransmitter dopamine—modulates the function of a subcortical brain area called the striatum.
Working with their very large collection of exquisitely curated and characterized donated human brains, researchers at the Institute seek to identify the mechanisms of action through which genetic variations associated with schizophrenia and other psychiatric illnesses actually cause the illnesses.
Schizophrenia is a highly complex illness with a genetic component that has proven very difficult to pinpoint in a manner that can guide the development of more effective treatments or even lead to a cure.
Robert Freedman, M.D., editor of the American Journal of Psychiatry (AJP) selected a paper by Rebecca Birnbaum, M.D., and colleagues as “particularly interesting and important” and featured it in the editors’ selection of noteworthy papers of 2014.
LIBD investigators led by CEO Daniel R. Weinberger, M.D - as members of the Schizophrenia Working Group (SWG) of the Psychiatric Genomics Consortium – are participating in the largest and expanding genetic study of schizophrenia to date.
A specific deletion on chromosome 22 (22q11.2 deletion syndrome or 22q11.2DS) is known to cause cognitive dysfunction and increase the risk for schizophrenia—particularly because of that deletion’s effect on the cathechol-O-methyltransferase (COMT) gene.
New nerve cells (neurons) are generated at an important rate throughout the human brain. This process, called “neurogenesis”, supports development of the brain’s intricate structures, myriad connections and establishment of its communication network.
There are many genetic factors involved in causing complex illnesses such as schizophrenia. There can be chromosomal deletions, inherited or non-inherited (“de novo”) mutations in genes, as well as the effects of combinations of normal genetic variation.