Garilyn Jentarra, Ph.D.

Associate Professor

College of Graduate Studies
Department of Biochemistry
Midwestern University
Agave Hall, 201-P
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


2017-current Associate Professor in Biochemistry Midwestern University, Glendale, AZ
2012-2017 Assistant Professor in Biochemistry Midwestern University, Glendale, AZ
2010-2012 Faculty Research Associate Barrow Neurological Institute, Phoenix, AZ
2004-2010 Post-Doctoral Fellow Barrow Neurological Institute, Phoenix, AZ
1999-2004 Research/Teaching Assistant Arizona State University, Tempe, AZ


2018-present Member, International Society to Advance Alzheimer's Research and Treatment
2005-present Member, Society for Neuroscience
2003-present Member, American Society for Microbiology
2000-present Member, American Society for Virology


Project 1:

My research into Alzheimer's disease (AD) focuses on two aspects: 1) the potential role of microbes in the development of AD and 2) the role of the AD risk gene, APOE4, in AD (the ε4 allele of apolipoprotein is the predominant risk factor for late-onset AD). My collaborators and I are using various methods to explore these two aspects. We have performed 16S rRNA gene sequencing of DNA extracted from the post-mortem tissue of AD patients and various control groups. In doing this, we have discovered that many varieties of microbes are present in the brains of individuals with AD and mild cognitive impairment (MCI) but not in the brains of non-demented control individuals. This implies that there may be damage to the blood-brain barrier in individuals with affected cognitive status, with this damage allowing microbes from the bloodstream to enter the brain. We propose that the presence of microbes drives the pathology observed in AD patients, including the activation of microglia and the deposition of amyloid beta, which recent data indicates can act as an anti-microbial peptide.

We are also using mouse models of AD (3xTG and APOE4 mice) to test whether infection can drive AD pathology or whether the APOE4 allele alters response to infection or compromises the blood-brain barrier. We hypothesize that infection with common microbes will drive more rapid development of AD-associated pathology in mice that are genetically engineered to develop it (3xTG mice). Further, we antipate that APOE4 mice will be more vulnerable to the entry of microbes into the brain and may potentially have stronger inflammatory responses.

In addition we have performed qPCR studies which identified significant changes in the expression of genes involved in synaptic plasticity and metabolism in young adult APOE4 carriers, which may be a possible mechanism by which the APOE4 allele creates a vulnerability to the development of AD, specifically in terms of learning and memory. 

Project 2:

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.

Selected Publications (See PubMed results)

  1. Perkins M, Wolf AB, Chavira B, Shonebarger D, Meckel JP, Leung L, Ballina L, Ly S, Saini A, Jones TB, Vallejo J, Jentarra G, Valla J. Altered energy metabolism pathways in the posterior cingulate in young adulty apolipoprotein E4 carriers. J Alzheimers Dis. 2016 Apr 23;53(1):95-106.
  2. 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.
  3. 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.
  4. 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.
  5. 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).
  6. 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.
  7. 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.
  8. Jentarra GM, Snyder SL, Narayanan V. Genetic Aspects of Neurocutaneous Disorders. Seminars in Pediatric Neurology 2006, 13:43-47.
  9. 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.