Garilyn Jentarra, Ph.D.

Assistant Professor

Arizona College of Osteopathic Medicine
Department of Biochemistry
Midwestern University
201, Agave Hall
19555 N 59th Ave
Glendale, AZ 85308

Office: 623-572-3334





Ph.D. Molecular and Cellular Biology Arizona State University 2004
B.S. Psychology Montana State University-Billings 1994


2012-current Assistant Professor in Biochemistry Midwestern University, Glendale, AZ
2010-2012 Faculty Research Associate Barrow Neurological Institute, Phoenix, AZ
2004-2010 Faculty Research Associate Post-Doctoral Fellow, Barrow Neurological Institute, Phoenix, AZ
1999-2004 Research/Teaching Assistant Arizona State University, Tempe, AZ


2005-present Member, Society for Neuroscience
2003-present Member, American Society for Microbiology
2000-present Member, American Society for Virology


Project 1:

Rett syndrome is an X-linked neurodevelopmental disorder resulting from MeCP2 gene mutations. This disorder is most often observed in girls as it is usually non-survivable in boys. Symptoms of Rett syndrome include microcephaly, loss of verbal skills, loss of purposeful hand movements, stereotyped hand movements, autism associated behaviors, serious motor deficits and growth abnormalities. MeCP2, a methyl-CpG DNA binding protein, is widely regarded as a regulator of gene transcription. Gene expression studies have provided evidence that many genes are dysregulated when MeCP2 function is compromised. Exactly how this leads to the characteristic features of RTT is currently unknown.

My lab is studying RTT using the MeCP2 A140V mouse model, which reproduces a pathogenic human mutation. While the A140V mutation does not specifically cause RTT in girls, it does cause an X-linked mental retardation syndrome in boys and can in some cases cause mild mental retardation in girls. The capacity to cause mental retardation and other symptoms in boys (microcephaly, delayed psychomotor development, dysarthric speech, gait impairments/ataxia, kyphoscoliosis) implies that the A140V mutation is disrupting a function important in neuronal development. That this mutation does not result in the full spectrum of RTT symptoms only makes it more interesting, as it may be disrupting a specific function of MeCP2 which can contribute to the pathology of RTT.

In the A140V mouse we've identified various abnormalities shared with other MeCP2 mutant mouse models, including increased brain cell packing density, decreased branching of neuronal dendrites, and motor abnormalities. These same pathological and functional abnormalities of the brain are observed in RTT patients. Our recent gene expression profiling in the A140V mouse model revealed dysregulation of a large subset of neurotransmitter receptor genes in the cerebellum. A smaller number of dysregulated genes were identified in the cortex and the pattern of dysregulation observed was very different from that seen in cerebellar tissue. The large differences in the gene dysregulation indicate that MeCP2 is functioning differently in these two brain regions and that the A140V mutation may be more disruptive in the cerebellum than in the cortex, at least in regards to neurotransmitter receptor expression.

Future research is aimed at using gene expression data from this model as well as other RTT mouse models to elucidate the mechanisms by which MeCP2 mutations result in abnormal brain development and function. We hope that this information will ultimately identify targets for therapeutic drug interventions for patients with RTT or X-linked mental retardation.

Project 2:

APOE4 (the ε4 allele of apolipoprotein E) is the predominant risk factor for late-onset Alzheimer's disease (AD). Our preliminary qPCR studies identified significant changes in the expression of genes involved in synaptic plasticity and metabolism in young adult APOE4 carriers, which may help to reveal the mechanism by which the APOE4 allele creates a vulnerability to the development of AD, specifically in terms of learning and memory. We are currently expanding gene expression studies to encompass addtional classes of genes whose expression may also affect AD risk.  Most recently, we have begun studies into the relationship between peripheral immunological factors and brain pathology using post-mortem tissue from AD patients. The goal of these studies is to elucidate the relationship between immunogical activation and the development and course of AD.

Selected Publications (See PubMed results)

Ma LY, Wu C, Jin Y, Gao M, Li GH, Turner D, Shen JX, Zhang SJ, Narayanan V, Jentarra G, Wu J. Electrophysiological phenotypes of MeCP2 A140V mutant mouse model. CNS Neurosci Ther. 2014 May;20(5):420-8.

Garilyn M Jentarra, Stephen Gabe Rice, Shannon Olfers, Chris Rajan, David Saffen and Vinodh Narayanan. Skewed allele-specific expression of the NF1 gene: A possible mechanism for phenotypic variability in NF1. J Child Neurol. 2012 Jun;27(6):695-702.

Garilyn M. Jentarra, Stephen G. Rice, Shannon Olfers, David Saffen and Vinodh Narayanan. Evidence for population variation in TSC1 and TSC2 gene expression. BMC Medical Genetics 2011, 12:29.

Garilyn M. Jentarra, Shannon L. Olfers, Stephen G. Rice, Nishit Srivastava, Gregg E. Homanics, Mary Blue, Sakkubai Naidu, and Vinodh Narayanan. Abnormalities of cell packing density and dendritic complexity in the MeCP2 A140V mouse model of Rett syndrome/X-linked mental retardation. Designated "Highly Accessed" in BMC Neuroscience 2010, 11(1):19).

Vijaysri S, Jentarra GM, Heck MC, Garvey K, Mercer AA, McInnes CJ, Jacobs BL. Vaccinia viruses with mutations in the E3L gene as potential replication-competent, attenuated vaccines: intra-nasal vaccination.  Vaccine 2008, 26(5):664-76.

Jentarra GM, Heck MC, Youn JW, Kibler K, Langland JO, Baskin CR, Ananieva O, Chang Y, Jacobs BL.  Vaccinia viruses with mutations in the E3L gene as potential replication-competent, attenuated vaccines: scarification vaccination.  Vaccine 2008, 26(23):2860-72.

Jentarra GM, Snyder SL, Narayanan V. Genetic Aspects of Neurocutaneous Disorders. Seminars in Pediatric Neurology 2006, 13:43-47.

Brandt T, Heck MC, Vijaysri S, Jentarra GM, Cameron JM, Jacobs BL. The N-terminal domain of the vaccinia virus E3L-protein is required for neurovirulence, but not induction of a protective immune response. Virology 2005, 333(2):263-70.