Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-05
Biography and Research Information
OverviewAI-generated summary
Orwa Aboud, an Assistant Professor at the University of Arkansas for Medical Sciences, investigates the molecular mechanisms and potential therapeutic targets for brain tumors, particularly gliomas and glioblastomas. His research employs advanced techniques, including metabolomics and machine learning, to characterize these complex diseases. Recent work has focused on identifying lipidomic signatures and analyzing mitochondrial ultrastructure in different glioma subtypes, aiming to uncover novel diagnostic and prognostic markers. Aboud also explores the efficacy of targeted therapies, such as Epidermal Growth Factor Receptor inhibitors and BRAF inhibitors, in treating specific mutations found in brain tumors and craniopharyngiomas. His scholarship includes 120 publications and 539 citations, with an h-index of 12. He collaborates with researchers at his institution, including Meenakshisundaram Balasubramaniam, W. Sue T. Griffin, Srinivas Ayyadevara, and Narasimhappagari Jagadeesh.
Metrics
- h-index: 12
- Publications: 120
- Citations: 562
Positions
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Assistant Professor 2020–presentUniversity of California Neurology and Neurological Surgery ORCID
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Assistant ProfessorUniversity of Arkansas for Medical Sciences ORCID
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National Institutes of Health 2018–2020Neuro Oncology Branch ORCID
Selected Publications
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Abstract LB131: The role of the proinflammatory cytokine IL-1β and its signaling cascade in glioblastoma pathogenesis and the therapeutic effect of IL-1RA and Tolcapone as anticancer agents (2025)
Collaboration Network
Top Collaborators
Robert E. Mrak
University of Toledo (US)
4 shared publications
- Loss of angiotensin II receptor expression in dopamine neurons in Parkinson’s disease correlates with pathological progression and is accompanied by increases in Nox4- and 8-OH guanosine-related nucleic acid oxidation and caspase-3 activation
- Epilepsy: neuroinflammation, neurodegeneration, and APOE genotype
- Apolipoprotein E expression is elevated by interleukin 1 and other interleukin 1-induced factors
- Aging, Alzheimer's, and APOE genotype influence the expression and neuronal distribution patterns of microtubule motor protein dynactin-P50
W. Sue T. Griffin
University of Arkansas for Medical Sciences
4 shared publications
In database
- Epilepsy: neuroinflammation, neurodegeneration, and APOE genotype
- Apolipoprotein E expression is elevated by interleukin 1 and other interleukin 1-induced factors
- Aging, Alzheimer's, and APOE genotype influence the expression and neuronal distribution patterns of microtubule motor protein dynactin-P50
- Abstract LB131: The role of the proinflammatory cytokine IL-1β and its signaling cascade in glioblastoma pathogenesis and the therapeutic effect of IL-1RA and Tolcapone as anticancer agents
Ling Liu
University of Arkansas for Medical Sciences
2 shared publications
In database
- Aging, Alzheimer's, and APOE genotype influence the expression and neuronal distribution patterns of microtubule motor protein dynactin-P50
- Abstract LB131: The role of the proinflammatory cytokine IL-1β and its signaling cascade in glioblastoma pathogenesis and the therapeutic effect of IL-1RA and Tolcapone as anticancer agents
Ayman Al-Salaimeh
University of Kentucky (US)
2 shared publications
- Discrepant Clinical Signs among Patients with Organic Neurological Disease -Prospective study (P4.180)
- Followup on Discrepant Clinical Signs among Patients with Organic Neurological Diseases (P2.191)
Kinshuk Sahaya
2 shared publications
- Discrepant Clinical Signs among Patients with Organic Neurological Disease -Prospective study (P4.180)
- Followup on Discrepant Clinical Signs among Patients with Organic Neurological Diseases (P2.191)
Archana Hinduja
The Ohio State University (US)
2 shared publications
- Discrepant Clinical Signs among Patients with Organic Neurological Disease -Prospective study (P4.180)
- Followup on Discrepant Clinical Signs among Patients with Organic Neurological Diseases (P2.191)
Paul A. Parcon
University of Arkansas for Medical Sciences (US)
1 shared publication
- Aging, Alzheimer's, and APOE genotype influence the expression and neuronal distribution patterns of microtubule motor protein dynactin-P50
K. Mark DeWall
Brigham Young University - Idaho (US)
1 shared publication
- Aging, Alzheimer's, and APOE genotype influence the expression and neuronal distribution patterns of microtubule motor protein dynactin-P50
Frederick A. Boop
University of Tennessee Health Science Center (US)
1 shared publication
- Epilepsy: neuroinflammation, neurodegeneration, and APOE genotype
Ling Liu
University of Arkansas for Medical Sciences (US)
1 shared publication
- Apolipoprotein E expression is elevated by interleukin 1 and other interleukin 1-induced factors
Richard A. Jones
University of Arkansas for Medical Sciences (US)
1 shared publication
- Apolipoprotein E expression is elevated by interleukin 1 and other interleukin 1-induced factors
Steven W. Barger
Central Arkansas Veterans Healthcare System
1 shared publication
In database
- Apolipoprotein E expression is elevated by interleukin 1 and other interleukin 1-induced factors
W. Michael Zawada
Institute on Aging (US)
1 shared publication
- Loss of angiotensin II receptor expression in dopamine neurons in Parkinson’s disease correlates with pathological progression and is accompanied by increases in Nox4- and 8-OH guanosine-related nucleic acid oxidation and caspase-3 activation
JoAnn Biedermann
Institute on Aging (US)
1 shared publication
- Loss of angiotensin II receptor expression in dopamine neurons in Parkinson’s disease correlates with pathological progression and is accompanied by increases in Nox4- and 8-OH guanosine-related nucleic acid oxidation and caspase-3 activation
Quinton D. Palmer
Institute on Aging
1 shared publication
In database
- Loss of angiotensin II receptor expression in dopamine neurons in Parkinson’s disease correlates with pathological progression and is accompanied by increases in Nox4- and 8-OH guanosine-related nucleic acid oxidation and caspase-3 activation
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