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303 E. Superior St.

Lurie 7-125

Chicago, IL 60611

 

676 N. Saint Clair St.

Suite 1260

Chicago, IL 60611

 

303 E. Chicago Ave.

Ward 9-148

Chicago, IL 60611

 

Ph: 312.503.5600

Fax: 312.503.5603

 

Faculty

Laura B. K. Herzing, Ph.D.
Assistant Professor, Dept. of Pediatrics
Northwestern University Feinberg School of Medicine
Program in Human Molecular Genetics
Children's Memorial Research Center (CMRC)

To contact Dr. Herzing:
2300 Children's Plaza Box 211
Chicago, IL 60614
Phone: (773) 755-6354
Fax: 773) 755-6345

e-mail:l-herzing@northwestern.edu

Dr. Herzing's website

PubMed Reference Lookup

 

Research Interests:


Dr. Herzing's work focuses on identifying epigenetic changes in gene expression that underlie neurodevelopmental disorders such as autism, Angelman and Rett syndromes, and epilepsy. Using both patient samples and mouse models of these disorders, her goal is to identify when the critical expression changes occur, and whether their effects can be reversed or improved. Rett Syndrome (RS) is a progressive neurologic disorder that has many clinical features in common with autism and Angelman syndrome (AS). Like children with autism, girls with RS often initially appear to develop normally, then lose or fail to gain milestones. A few children born with AS carry a mutation in MeCP2, the gene associated with RS, although most carry a deletion of the UBE3A gene. Dr. Herzing has demonstrated that there is also a developmental and tissue-specific alteration in expression of Ube3a and adjacent genes in RS and RS mouse models, which could explain the phenotypic overlap between AS, RS and autism. These genes, several of which are imprinted, are also duplicated in as many as 2% of patients with autism, and Dr. Herzing has shown that these patients exhibit enhanced expression of these genes. Working on the hypothesis that misregulation, rather than mutation, of the candidate UBE3A, ATP10C and GABRB3 genes leads to autism, Dr. Herzing is using transgenic and RNAi technologies to lower or elevate the expression of these genes in mouse models. Careful assessment of resultant behavioral alterations will permit determination of the role such candidate genes have in the development of autism. These animals will also serve as vehicles to validate treatments and therapies for autism in a model system based on human etiology.


Many children with these disorders also develop seizures, and epilepsies in general remain a major childhood medical concern. The development of most pediatric epilepsies is likely influenced by a change in expression of ion-channel genes. Dr. Herzing is working to expand a collaboration with The University of Chicago and Milwaukee Childrens Hospital, to facilitate ion-channel gene expression studies in tissue recovered from patients undergoing epilepsy surgery. Results from these studies will inform the development and interrogation of animal models for seizure development, and will help define the mechanisms underlying idiopathic epilepsy and seizures associated with syndromes and disorders such as autism, RS and AS.




 

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