Jessica M Van Baaren

Publications (2)8.04 Total impact

• Article: Derivation of autism spectrum disorder-specific induced pluripotent stem cells from peripheral blood mononuclear cells.

  Brooke A DeRosa, Jessica M Van Baaren, Gaurav K Dubey, Joycelyn M Lee, Michael L Cuccaro, Jeffery M Vance, Margaret A Pericak-Vance, Derek M Dykxhoorn
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  ABSTRACT: Induced pluripotent stem cells (iPSCs) hold tremendous potential both as a biological tool to uncover the pathophysiology of disease by creating relevant cell models and as a source of stem cells for cell-based therapeutic applications. Typically, iPSCs have been derived by the transgenic overexpression of transcription factors associated with progenitor cell or stem cell function in fibroblasts derived from skin biopsies. However, the need for skin punch biopsies to derive fibroblasts for reprogramming can present a barrier to study participation among certain populations of individuals, including children with autism spectrum disorders (ASDs). In addition, the acquisition of skin punch biopsies in non-clinic settings presents a challenge. One potential mechanism to avoid these limitations would be the use of peripheral blood mononuclear cells (PBMCs) as the source of the cells for reprogramming. In this article we describe, for the first time, the derivation of iPSC lines from PBMCs isolated from the whole blood of autistic children, and their subsequent differentiation in GABAergic neurons.
  Neuroscience Letters 03/2012; 516(1):9-14. · 2.11 Impact Factor
• Article: Vitamin D receptor and Alzheimer's disease: a genetic and functional study.

  Liyong Wang, Kenju Hara, Jessica M Van Baaren, Justin C Price, Gary W Beecham, Paul J Gallins, Patrice L Whitehead, Gaofeng Wang, Chunrong Lu, Michael A Slifer, Stephan Züchner, Eden R Martin, Deborah Mash, Jonathan L Haines, Margaret A Pericak-Vance, John R Gilbert
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  ABSTRACT: Genetic studies on late-onset Alzheimer's disease (AD) have repeatedly mapped susceptibility loci onto chromosome 12q13, encompassing the vitamin D receptor (VDR) gene. Epidemiology studies have indicated vitamin D insufficiency as a risk factor for AD. Given that VDR is the major mediator for vitamin D's actions, we sought to clarify the role of VDR in late-onset AD. We conducted an association study in 492 late-onset AD cases and 496 controls with 80 tagging single nucleotide polymorphisms (SNPs). The strongest association was found at a promoter SNP rs11568820 (P = 9.1 × 10(-6), odds ratio (OR) = 1.69), which resides within the transcription factor Cdx-2 binding site and the SNP has been also known as CDX2. The risk-allele at rs11568820 is associated with lower VDR promoter activity (p < 10(-11)). The overexpression of VDR or vitamin D treatment suppressed amyloid precursor protein (APP) transcription in neuroblastoma cells (p < 0.001). We provide both statistical evidence and functional data suggesting VDR confers genetic risk for AD. Our findings are consistent with epidemiology studies suggesting that vitamin D insufficiency increases the risk of developing AD.
  Neurobiology of aging 02/2012; 33(8):1844.e1-9. · 5.94 Impact Factor