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Home | Pregnancy Timeline | News Alerts |News Archive Oct 16, 2014

(LEFT) Young neurons in the dentate gyrus part of the brain in a normal mouse (green)
and (RIGHT) a sibling with Kabuki syndrome-like condition.

http://www.nature.com/nrm/journal/v10/n3/box/nrm2640_BX1.html







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Cancer drug eases mental illness in mice

Johns Hopkins research reports an anticancer drug helps "unwind" DNA in mice with a mental disorder similar to that found in Kabuki syndrome — an inherited intellectual disorder of humans — improving memory function of those mice.

Kabuki syndrome is a genetic mutation causing errors in compression of the DNA strand to make it fit within a cell. In mice with a similar Kabuki like condition, researchers found errors led to a persistent decrease in new cell growth in the dentate gyrus part of the brain. These two findings add to growing evidence that not all intellectual disabilities are irreversible.


The term "Mendelian disorders of the epigenetic machinery" in the last ten years has been given to multiple congenital and intellectual disabilities which follow Mendalian inheritance — but result from epigenetic (or outside the gene) mutations.

Some disorders fitting this discription are Kabuki, Rett and Rubenstein-Taybi syndromes, and molecular defects in the methyl-CpG-binding domain protein 5 (MDB5) gene identified in some autistic spectrum children.

According to the National Center for Biotechnology Information, USA, many more epigentic disorders will likely be identified with increasing advances in genetic sequencing. http://www.ncbi.nlm.nih.gov/pubmed/25184531


The research appeared online Oct. 1 in the journal Science Translational Medicine.


"Mendelian disorders of epigenetic machinery affect how DNA is 'packaged' to fit into a cell. Finding that a drug can ease some of the symptoms in this group of disorders suggests that other Mendelian disorders in histone machinery may be similarly treatable."

Hans Bjornsson, M.D., Ph.D., an assistant professor of pediatrics and genetics in the Johns Hopkins University School of Medicine's McKusick-Nathans Institute of Genetic Medicine.


Kabuki syndrome is caused by mutations in one of two genes that govern how tightly DNA wraps itself to fit within a cell. In order to read tightly wound DNA and put it to use in making new proteins, chromatin must temporarily relax and open up a DNA strand to be "read."

Specialized enzymes, called "writers" (which add) and "erasers" (which subtract), induce chemicals to open or close chromatin proteins.

Previous research had found that Kabuki syndrome can result from mutations to one of two genes — a writer or an eraser — with the net effect chromatin does not operate correctly. That finding led Bjornsson and his collaborators to suspect Kabuki and similar syndromes might be the result of an imbalance between chromatin's open and closed states.

If true, Bjornsson feels disorders in histone machinery might be treatable by balancing chromatin's openning and closing.

To test the idea, Joel Benjamin, a graduate student in Bjornsson's lab, experimented with mice having a mutation in one of their genes similar to what appears in humans with Kabuki syndrome.


"Kabuki" mice in their young adult phase of growth, were treated with AR-42, a drug developed for cancers of the blood known to open up compacted chromatin.

After two weeks of treatment, the mice were tested in the Morris water maze to measure their affectiveness at memory creation. AR-42 treated mice performed better than untreated mice — about as well as healthy mice.


Microscopically examining the brains of AR-42 treated mice, researchers saw they had more newly formed neurons in a part of the hippocampus called the dentate gyrus.


"The dentate gyrus is important for memory formation, and it's also one of the few places in adult brains where we see new neurons. We think that when DNA's chromatin opens up, the cells are able to 'turn on' one or more genes needed for new neuron growth."

Hans Bjornsson, M.D., Ph.D., an assistant professor of pediatrics and genetics in the Johns Hopkins University School of Medicine's McKusick-Nathans Institute of Genetic Medicine.


Physicians generally consider intellectual disability that accompanies disorders like Kabuki syndrome to be irreversible, Bjornsson notes. "But we now know that new brain cells continue to form throughout our lives. If Kabuki syndrome and related disorders cause fewer neurons to be made in adulthood, stimulating neuron growth may be an effective strategy for treating intellectual disability," he says.


In Scotland, a research group has also reported a way to reverse neurological dysfunction in mice with a condition similar to Rett syndrome, another inherited disorder causing intellectual disability.

However, treatment for any inborn intellectual disability in people could still take a decade or more to develop, Bjornsson cautions.


Bjornsson's next step will be to focus his research on the dentate gyrus to see whether it is the primary source of memory defects found in Kabuki mice. He would then like to explore whether there are other potential drugs having a similar effect to AR-42.

Abstract
Kabuki syndrome is caused by haploinsufficiency for either of two genes that promote the opening of chromatin. If an imbalance between open and closed chromatin is central to the pathogenesis of Kabuki syndrome, agents that promote chromatin opening might have therapeutic potential. We have characterized a mouse model of Kabuki syndrome with a heterozygous deletion in the gene encoding the lysine-specific methyltransferase 2D (Kmt2d), leading to impairment of methyltransferase function. In vitro reporter alleles demonstrated a reduction in histone 4 acetylation and histone 3 lysine 4 trimethylation (H3K4me3) activity in mouse embryonic fibroblasts from Kmt2d+/βGeo mice. These activities were normalized in response to AR-42, a histone deacetylase inhibitor. In vivo, deficiency of H3K4me3 in the dentate gyrus granule cell layer of Kmt2d+/βGeo mice correlated with reduced neurogenesis and hippocampal memory defects. These abnormalities improved upon postnatal treatment with AR-42. Our work suggests that a reversible deficiency in postnatal neurogenesis underlies intellectual disability in Kabuki syndrome.

Bjornsson led the study in collaboration with Harry "Hal" Dietz, M.D., the Victor A. McKusick Professor of Medicine and Genetics and director of the William S. Smilow Center for Marfan Syndrome Research and heads the McKusick-Nathans Epigenetics and Chromatin Clinic.

Copyright © 2014, American Association for the Advancement of Science

Other authors on the paper were Li Zhang, Elizabeth E. Gerber, Yi-Chun Chen, Michelle C. Potter and Kasper D. Hansen of The Johns Hopkins University; and Jacqueline Weissman and Rebecca Vaurio of the Kennedy Krieger Institute.

This work was supported by the William S. Smilow Center for Marfan Syndrome Research, the Howard Hughes Medical Institute, the National Institutes of Health's Director's Early Independence Award (grant number DP5OD017877) and the American Academy of Pediatrics' Section on Genetics and Birth Defects.

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