Steven W. Barger
Professor
Also affiliated: United States Department of Veterans Affairs (2006); University of Kentucky (1993–1996); University of Colorado Boulder (1998); Vanderbilt University (1989–1992); British Geriatrics Society (1998); University of Arkansas Medical Center (1997–2023); University of Colorado System (1998); Stephens College (2007); Arkansas Cardiology (2002–2006); Central Arkansas Veterans Healthcare System (1999–2026); Geriatric Research Education and Clinical Center (1997–2026); Institute on Aging (2013–2017); National Institute on Aging (1996); John L. McClellan Memorial Veterans Hospital (1997–1999); Reynolds American (United States) (2017); Arkansas Department of Agriculture (2020); University of Toledo (2014)
Faculty Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Steven W. Barger's research program focuses on the molecular and cellular mechanisms underlying neurodegenerative diseases, particularly Alzheimer's disease. His work investigates the role of cellular processes such as autophagy and lysosomal function, as well as metabolic pathways like glucose transport and glutamate regulation, in disease pathogenesis. Barger has received federal funding from the NIH/National Institute on Aging for projects examining the role of glucose transport in Alzheimer's disease and the compromised function of a glial glucose transporter in aging and Alzheimer's disease, totaling over $750,000.
His laboratory group has published research exploring therapeutic strategies, including the development of small molecules to rescue autophagic failure and inhibitors of system xC− transport to reduce microglial glutamate release and neurotoxicity. Other studies have investigated the potential of liraglutide to counteract endoplasmic reticulum stress in neurons and examined the association of P-glycoprotein substrates with Alzheimer's disease risk. Barger's work also extends to exploring how specific protein fragments, such as the central repeat fragment of reelin, can impact neuronal signaling and cognitive function.
With an h-index of 50 and over 10,000 citations across 142 publications, Barger is recognized as a highly cited researcher. He collaborates with researchers at the University of Arkansas for Medical Sciences and the University of Arkansas at Little Rock. His lab maintains an active website and leads a research group dedicated to advancing the understanding and treatment of neurodegenerative disorders.
Metrics
- h-index: 50
- Publications: 141
- Citations: 10,363
Selected Publications
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Insulin Growth Factor 1 affects glutamate receptor activity differently in primary cultures of neocortical versus hippocampal neurons (2026)
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Impact of P-glycoprotein substrates on transendothelial transport of amyloid-β peptide in an in vitro model (2026)
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Modulation of apolipoprotein E receptor-2 by ApoE4, amyloid β-peptide, reelin, and secreted amyloid precursor protein: a common point of impact in Alzheimer’s disease pathogenesis (2026)
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Microglial serine racemase knockout alleviates Alzheimer-like neuropathology and behavioral deficit via lactylation-mediated anti-inflammation (2026)
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Impact of P-Glycoprotein Substrates on Transendothelial Transport of Amyloid-β Peptide (2025)
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Prescription-based association of P-glycoprotein substrates with Alzheimer's disease risk: A nested case-control study (2025)
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P-glycoprotein and Alzheimer’s Disease: Threats and Opportunities (2025)
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Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules (2024)
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Design, synthesis, and characterization of novel system xC− transport inhibitors: inhibition of microglial glutamate release and neurotoxicity (2023)
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Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan (2023)
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Central repeat fragment of reelin leads to active reelin intracellular signaling and rescues cognitive deficits in a mouse model of reelin deficiency (2023)
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Design, synthesis, and characterization of novel Xc- transport inhibitors: Inhibition of microglial glutamate release and neurotoxicity (2023)
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Amyloid β-Peptide Effects on Glucose Regulation Are Dependent on Apolipoprotein E Genotype (2023)
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Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis (2022)
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Glucose transport in the regulation of T-cell activation: the journey may be as important as the destination (2022)
Federal Grants 2 $754,900 total
Role of glucose transport in Alzheimer's disease pathogenesis
Compromised function of a glial glucose transporter in aging and Alzheimer's disease
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Molecular aspects of endocrine and metabolic dysregulation in neurodegeneration NIH/NIA
- Neuroscience Research Center Core Facility at UAMS NIH
- Secreted Alzheimer amyloid precursor protein (sAPP) antagonizes Reelin receptors NIH
- CYCLIC GMP AND KB-DEPENDENT TRANSCRIPTION IN NEURONS NIH
- TO ESTABLISH UAMS ACCOUNT FOR SALARY SUPPORT OF XIANRONG MAO. INVOICE U OF A FOUNDATION OFFICE University of Arkansas Foundation
- Destablization of LRP family receptors by Alzheimer-related presenilin mutations NIH
- PPG Core C: Molecular Analysis NIH/NIA
- Inference of Common Pathways Underlying Neurodegeneration & Other Age-Progressive Diseases - Continuation - Continuation NIH/Nat. Inst. on Aging
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences
- BALANCED BIOACTIVITY OF ALZHEIMER BETA AMYLOID PRECURSOR NIH
- Sp1, kappa-B enhancers and transcriptions in neurons NIH
- CYCLIC GMP--MEDIATOR OF BETA-AMYLOID PRECURSOR FUNCTION NIH
- Early Events in Alzheimer Pathogenesis NIH
Collaboration Network
Top Collaborators
- Prescription-based association of P-glycoprotein substrates with Alzheimer's disease risk: A nested case-control study
- P-glycoprotein and Alzheimer’s Disease: Threats and Opportunities
- Impact of P-Glycoprotein Substrates on Transendothelial Transport of Amyloid-β Peptide
- Amyloid β-Peptide Effects on Glucose Regulation Are Dependent on Apolipoprotein E Genotype
- Amyloid β-peptide impacts on glucose regulation are dependent on apolipoprotein E genotype
- Amyloid β-Peptide Effects on Glucose Regulation Are Dependent on Apolipoprotein E Genotype
- Amyloid β-peptide impacts on glucose regulation are dependent on apolipoprotein E genotype
- Design, synthesis, and characterization of novel system xC− transport inhibitors: inhibition of microglial glutamate release and neurotoxicity
- Design, synthesis, and characterization of novel Xc- transport inhibitors: Inhibition of microglial glutamate release and neurotoxicity
- Central repeat fragment of reelin leads to active reelin intracellular signaling and rescues cognitive deficits in a mouse model of reelin deficiency
- Modulation of apolipoprotein E receptor-2 by ApoE4, amyloid β-peptide, reelin, and secreted amyloid precursor protein: a common point of impact in Alzheimer’s disease pathogenesis
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Serine Racemase Expression Differentiates Aging from Alzheimer’s Brain
- Serine Racemase Expression Differentiates Aging from Alzheimer’s Brain
- Serine Racemase Expression Differentiates Aging from Alzheimer’s Brain
- Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis
- Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis
- Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis
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