Sara E. Gombash

ORCID: 0000-0001-6026-9966
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About
Contact & Profiles
Research Areas
  • Virus-based gene therapy research
  • Parkinson's Disease Mechanisms and Treatments
  • Neurogenetic and Muscular Disorders Research
  • Neurological disorders and treatments
  • Nerve injury and regeneration
  • Congenital gastrointestinal and neural anomalies
  • Congenital Anomalies and Fetal Surgery
  • Calpain Protease Function and Regulation
  • Viral Infectious Diseases and Gene Expression in Insects
  • Transcranial Magnetic Stimulation Studies
  • RNA Interference and Gene Delivery
  • Viral gastroenteritis research and epidemiology
  • Muscle Physiology and Disorders
  • Botulinum Toxin and Related Neurological Disorders
  • Gastrointestinal disorders and treatments
  • Infectious Encephalopathies and Encephalitis
  • Gastrointestinal motility and disorders
  • RNA regulation and disease
  • Energy Harvesting in Wireless Networks
  • Whipple's Disease and Interleukins
  • Reproductive System and Pregnancy
  • Intestinal Malrotation and Obstruction Disorders
  • Neuroscience and Neural Engineering
  • Cardiac Structural Anomalies and Repair
  • Cardiovascular Issues in Pregnancy

The Ohio State University
2014-2022

Michigan State University
2011-2017

The Ohio State University Wexner Medical Center
2015

University of Cincinnati
2010-2015

Michigan United
2013

The mechanisms underlying the effects of long-term deep brain stimulation subthalamic nucleus (STN DBS) as a therapy for Parkinson's disease (PD) remain poorly understood. present study examined whether functionally effective, ST

10.3233/jpd-2011-11008 article EN Journal of Parkinson s Disease 2011-01-01

The discovery of the involvement alpha-synuclein (α-syn) in Parkinson's disease (PD) pathogenesis has resulted development and use viral vector-mediated α-syn overexpression rodent models. goal these series experiments was to characterize neurodegeneration functional deficits resulting from injection recombinant adeno-associated virus (rAAV) serotype 2/5-expressing human wildtype rat substantia nigra (SN). Rats were unilaterally injected into two sites SN with either rAAV2/5-expressing green...

10.1371/journal.pone.0081426 article EN cc-by PLoS ONE 2013-11-27

Proximal spinal muscular atrophy (SMA) is the most frequent cause of hereditary infant mortality. SMA an autosomal recessive neuromuscular disorder that results from loss Survival Motor Neuron 1 (SMN1) gene and retention SMN2 gene. The produces insufficient amount full-length SMN protein in motor neurons cord subsequent muscle paralysis. Previously we have shown overexpression human mouse ameliorates phenotype while skeletal had no effect. Using Cre recombinase, here show either deletion or...

10.1093/hmg/ddv283 article EN public-domain Human Molecular Genetics 2015-07-23

Gene therapies for neurological diseases with autonomic or gastrointestinal involvement may require global gene expression. Gastrointestinal complications are often associated Parkinson's disease and autism. Lewy bodies, a pathological hallmark of brains, routinely identified in the neurons enteric nervous system (ENS) following colon biopsies from patients. The ENS is intrinsic gut, responsible coordinating secretory motor functions tract. dysfunction can cause severe patient discomfort,...

10.3389/fnmol.2014.00081 article EN cc-by Frontiers in Molecular Neuroscience 2014-10-15

The 2007 Consensus Statement for Standard of Care in Spinal Muscular Atrophy (SMA) notes that patients suffer from gastroesophageal reflux, constipation and delayed gastric emptying. We used two mouse models SMA to determine whether functional GI complications are a direct consequence or secondary survival motor neuron (Smn) deficiency. Our results show despite normal activity levels food water intake, Smn deficiency caused constipation, emptying, slow intestinal transit reduced colonic...

10.1093/hmg/ddv127 article EN public-domain Human Molecular Genetics 2015-04-09

Spinal Muscular Atrophy (SMA) is an autosomal recessive disorder characterized by loss of lower motor neurons. SMA caused deletion or mutation the Survival Motor Neuron 1 (SMN1) gene and retention SMN2 gene. The SMN1 results in reduced levels SMN protein. appear to be particularly important neurons; however above that produced two copies have been suggested muscle. Studying spatial requirement both understanding how deficiency causes development effective therapies. Using Myf5-Cre, a...

10.1093/hmg/ddv332 article EN Human Molecular Genetics 2015-08-13

Abstract Subthalamic nucleus deep brain stimulation (STN DBS) protects dopaminergic neurons of the substantia nigra pars compacta (SNpc) against 6-OHDA and MPTP. We evaluated STN DBS in a parkinsonian model that displays α-synuclein pathology using unilateral, intranigral injections recombinant adeno-associated virus pseudotype 2/5 to overexpress wildtype human (rAAV2/5 α-syn). A low titer rAAV2/5 α-syn results progressive forelimb asymmetry, loss striatal terminal density modest SNpc...

10.1038/s41598-017-16690-x article EN cc-by Scientific Reports 2017-11-21

Neurotrophic factors are integrally involved in the development of nigrostriatal system and combination with gene therapy, possess great therapeutic potential for Parkinson's disease (PD). Pleiotrophin (PTN) is development, maintenance, repair dopamine (DA) system. The present study examined ability striatal PTN overexpression, delivered via psueudotyped recombinant adeno-associated virus type 2/1 (rAAV2/1), to provide neuroprotection functional restoration from 6-hydroxydopamine (6-OHDA)....

10.1038/mt.2011.216 article EN cc-by-nc-nd Molecular Therapy 2011-10-18

10.1007/978-1-4939-3271-9_16 article EN Methods in molecular biology 2015-11-26

We previously reported that systemic injection of AAV9 in aged mice (P550) results significantly fewer transduced CNS cells compared to adult (P49). This was not due the presence neutralizing antibodies mice. To determine whether aging brain and/or periphery is responsible for this reduction, we quantified transduction following stereotaxic or Aged male Balb/c (n = 6, P550) and 7, P50) received direct injections into striatum ipsilateral hippocampus with scAAV9-CB expressing green...

10.1016/s1525-0016(16)33427-x article EN cc-by-nc-nd Molecular Therapy 2016-05-01

We previously reported that intravenous delivery of AAV8 or AAV9 produces robust transduction in the enteric nervous system (ENS) mice is capsid dependent. The current proof-of-concept studies were to determine if AAV transduces ENS two higher species, specifically guinea pigs, a commonly used species for physiology studies, and cynomolgus macaques. Neonatal piglets (P2) intravenously injected with either scAAV8 (2.8-3.1×1010 vg/g) scAAV9-CB (2.8-3.4×1010 expressing green fluorescent protein...

10.1016/s1525-0016(16)33420-7 article EN cc-by-nc-nd Molecular Therapy 2016-05-01

To investigate novel genes involved in functional gastrointestinal disorders, we disrupted a master regulator of mRNA splicing, the survival motor neuron (SMN) protein. SMN disruption leads to widespread changes gene expression but has not been evaluated for effects (GI) tract. Mice with Nestin‐cre transgene were crossed cre reporter mice analyze enteric nervous system (ENS). Gene was detected excitatory and sensory neurons, interneurons, intraganglionic glia throughout myenteric plexus...

10.1096/fasebj.29.1_supplement.1002.16 article EN The FASEB Journal 2015-04-01
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