Match tier
Confirmed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-05
H
Héctor Rosas-Hernández
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Staff Fellow
Also affiliated: United States Food and Drug Administration (2013–2026); Autonomous University of San Luis Potosí (2009–2017)
20 h-index
44 pubs
1,017 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Héctor Rosas-Hernández's research focuses on the toxicological effects of nanoparticles and other substances on biological systems, with a particular emphasis on the central nervous system and cardiovascular system. He has investigated the impact of silver nanoparticles (AgNPs) on coronary endothelial cells and rat aortic rings, as well as the role of iron oxide nanoparticles in dopaminergic damage and neuronal injury. His work has also explored the disruption of the blood-brain barrier by amyloid beta peptides and the differential cytotoxic effects of various psychoactive substances on bovine brain microvessel endothelial cells.
Rosas-Hernández has also contributed to understanding the mechanisms of vascular tone regulation, examining the role of prolactin family hormones in nitric oxide and prostacyclin production in rat aortic rings. His research interests extend to the molecular underpinnings of neurological disorders, including protein kinases and their relation to Parkinson's disease. He leads a research group and has collaborated with researchers at the National Center for Toxicological Research, including Katelin S. Matazel and W. Drew Gill, with whom he shares multiple publications. His scholarship metrics include an h-index of 20, with over 1,000 citations across 63 publications.
Metrics
- h-index: 20
- Publications: 44
- Citations: 1,017
Positions
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Staff Fellow 2018–presentNational Center for Toxicological Research Division of Neurotoxicology ORCID
Selected Publications
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Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model (2026)
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Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model (2026)
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Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model (2026)
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Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model (2026)
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Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model (2026)
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Neurobehavioral and neurochemical effects of perinatal arsenite exposure in Sprague-Dawley rats (2021)
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Can SARS-CoV-2 infect the central nervous system via the olfactory bulb or the blood-brain barrier? (2021)
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Modification of methods to use Congo-red stain to simultaneously visualize amyloid plaques and tangles in human and rodent brain tissue sections (2020)
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Impaired Amyloid Beta Clearance and Brain Microvascular Dysfunction are Present in the Tg-SwDI Mouse Model of Alzheimer’s Disease (2020)
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Dr. Daniel Acosta and In Vitro toxicology at the U.S. Food and Drug Administration's National Center for Toxicological Research (2019)
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P4‐064: EVALUATION OF TAU NEUROPATHOLOGY AND OTHER KEY PROTEINS IN THE OLFACTORY BULB AND ITS CORRELATION WITH HIPPOCAMPUS IN HUMAN ALZHEIMER'S DISEASE (2019)
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Stretch-Induced Deformation as a Model to Study Dopaminergic Dysfunction in Traumatic Brain Injury (2019)
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Amyloid Beta 25–35 induces blood-brain barrier disruption in vitro (2019)
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Characterization of Serum Exosomes from a Transgenic Mouse Model of Alzheimer’s Disease (2019)
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Cytotoxicity profile of pristine graphene on brain microvascular endothelial cells (2019)
Collaboration Network
Top Collaborators
Elvis Cuevas
National Center for Toxicological Research (US)
22 shared publications
- Can SARS-CoV-2 infect the central nervous system via the olfactory bulb or the blood-brain barrier?
- Iron Oxide Nanoparticles Induce Dopaminergic Damage: In vitro Pathways and In Vivo Imaging Reveals Mechanism of Neuronal Damage
- Amyloid Beta 25–35 induces blood-brain barrier disruption in vitro
- Methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxypyrovalerone (MDPV) induce differential cytotoxic effects in bovine brain microvessel endothelial cells
- Protein Kinases and Parkinson’s Disease
Showing 5 of 22 shared publications
Syed F. Ali
National Center for Toxicological Research
18 shared publications
In database
- Iron Oxide Nanoparticles Induce Dopaminergic Damage: In vitro Pathways and In Vivo Imaging Reveals Mechanism of Neuronal Damage
- Amyloid Beta 25–35 induces blood-brain barrier disruption in vitro
- Methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxypyrovalerone (MDPV) induce differential cytotoxic effects in bovine brain microvessel endothelial cells
- Protein Kinases and Parkinson’s Disease
- Silver nanoparticles induce anti-proliferative effects on airway smooth muscle cells. Role of nitric oxide and muscarinic receptor signaling pathway
Showing 5 of 18 shared publications
Susan M. Lantz
National Center for Toxicological Research
13 shared publications
In database
- Methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxypyrovalerone (MDPV) induce differential cytotoxic effects in bovine brain microvessel endothelial cells
- Protein Kinases and Parkinson’s Disease
- Isolation and Culture of Brain Microvascular Endothelial Cells for In Vitro Blood-Brain Barrier Studies
- Changes in the metabolome and microRNA levels in biological fluids might represent biomarkers of neurotoxicity: A trimethyltin study
- Characterization of Biaxial Stretch as an In Vitro Model of Traumatic Brain Injury to the Blood-Brain Barrier
Showing 5 of 13 shared publications
Merle G. Paule
National Center for Toxicological Research
12 shared publications
In database
- Iron Oxide Nanoparticles Induce Dopaminergic Damage: In vitro Pathways and In Vivo Imaging Reveals Mechanism of Neuronal Damage
- Methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxypyrovalerone (MDPV) induce differential cytotoxic effects in bovine brain microvessel endothelial cells
- Protein Kinases and Parkinson’s Disease
- Isolation and Culture of Brain Microvascular Endothelial Cells for In Vitro Blood-Brain Barrier Studies
- Characterization of Biaxial Stretch as an In Vitro Model of Traumatic Brain Injury to the Blood-Brain Barrier
Showing 5 of 12 shared publications
Sumit Sarkar
National Center for Toxicological Research
12 shared publications
In database
- Iron Oxide Nanoparticles Induce Dopaminergic Damage: In vitro Pathways and In Vivo Imaging Reveals Mechanism of Neuronal Damage
- Amyloid Beta 25–35 induces blood-brain barrier disruption in vitro
- Protein Kinases and Parkinson’s Disease
- Modification of methods to use Congo-red stain to simultaneously visualize amyloid plaques and tangles in human and rodent brain tissue sections
- Impaired Amyloid Beta Clearance and Brain Microvascular Dysfunction are Present in the Tg-SwDI Mouse Model of Alzheimer’s Disease
Showing 5 of 12 shared publications
Syed Z. Imam
National Center for Toxicological Research
9 shared publications
In database
- Iron Oxide Nanoparticles Induce Dopaminergic Damage: In vitro Pathways and In Vivo Imaging Reveals Mechanism of Neuronal Damage
- Amyloid Beta 25–35 induces blood-brain barrier disruption in vitro
- Changes in the metabolome and microRNA levels in biological fluids might represent biomarkers of neurotoxicity: A trimethyltin study
- Characterization of Biaxial Stretch as an In Vitro Model of Traumatic Brain Injury to the Blood-Brain Barrier
- Characterization of uniaxial high-speed stretch as an in vitro model of mild traumatic brain injury on the blood-brain barrier
Showing 5 of 9 shared publications
Bonnie Robinson
National Center for Toxicological Research
7 shared publications
In database
- Iron Oxide Nanoparticles Induce Dopaminergic Damage: In vitro Pathways and In Vivo Imaging Reveals Mechanism of Neuronal Damage
- Impaired Amyloid Beta Clearance and Brain Microvascular Dysfunction are Present in the Tg-SwDI Mouse Model of Alzheimer’s Disease
- Changes in the metabolome and microRNA levels in biological fluids might represent biomarkers of neurotoxicity: A trimethyltin study
- Identification of altered microRNAs in serum of a mouse model of Parkinson’s disease
- Characterization of Serum Exosomes from a Transgenic Mouse Model of Alzheimer’s Disease
Showing 5 of 7 shared publications
James Raymick
National Center for Toxicological Research
6 shared publications
In database
- Modification of methods to use Congo-red stain to simultaneously visualize amyloid plaques and tangles in human and rodent brain tissue sections
- Impaired Amyloid Beta Clearance and Brain Microvascular Dysfunction are Present in the Tg-SwDI Mouse Model of Alzheimer’s Disease
- Changes in the metabolome and microRNA levels in biological fluids might represent biomarkers of neurotoxicity: A trimethyltin study
- Identification of altered microRNAs in serum of a mouse model of Parkinson’s disease
- Characterization of Serum Exosomes from a Transgenic Mouse Model of Alzheimer’s Disease
Showing 5 of 6 shared publications
Manuel Alejandro Ramirez-Lee
National Center for Toxicological Research
5 shared publications
In database
- Can SARS-CoV-2 infect the central nervous system via the olfactory bulb or the blood-brain barrier?
- Amyloid Beta 25–35 induces blood-brain barrier disruption in vitro
- Silver nanoparticles induce anti-proliferative effects on airway smooth muscle cells. Role of nitric oxide and muscarinic receptor signaling pathway
- Cytotoxicity profile of pristine graphene on brain microvascular endothelial cells
- Silver nanoparticles Induce Anti-Proliferative Effects on Airway Smooth Muscle Cells. Role of Nitric Oxide and Muscarinic Receptor Signaling Pathway
William Slikker
National Center for Toxicological Research
5 shared publications
In database
- Changes in the metabolome and microRNA levels in biological fluids might represent biomarkers of neurotoxicity: A trimethyltin study
- Characterization of Biaxial Stretch as an In Vitro Model of Traumatic Brain Injury to the Blood-Brain Barrier
- Characterization of uniaxial high-speed stretch as an in vitro model of mild traumatic brain injury on the blood-brain barrier
- Dr. Daniel Acosta and In Vitro toxicology at the U.S. Food and Drug Administration's National Center for Toxicological Research
- Neurovascular unit components on a chip as a model to study traumatic brain injury
Katelin S. Matazel
National Center for Toxicological Research
5 shared publications
In database
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
W. Drew Gill
National Center for Toxicological Research
5 shared publications
In database
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
Lorna Ewart
Emulate (United States) (US)
5 shared publications
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
Randy S. Daughters
Emulate (United States) (US)
5 shared publications
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
- Additional file 1 of Modeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model
Joseph P. Hanig
Center for Drug Evaluation and Research (US)
4 shared publications
- Modification of methods to use Congo-red stain to simultaneously visualize amyloid plaques and tangles in human and rodent brain tissue sections
- Changes in the metabolome and microRNA levels in biological fluids might represent biomarkers of neurotoxicity: A trimethyltin study
- Identification of altered microRNAs in serum of a mouse model of Parkinson’s disease
- Characterization of Serum Exosomes from a Transgenic Mouse Model of Alzheimer’s Disease
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