Steven W. Barger
Professor
faculty
Research Areas
Biography and Research Information
OverviewAI-generated summary
Steven W. Barger's research focuses on the pathogenesis of Alzheimer's disease and other neurodegenerative conditions. He has served as PI on two NIH/National Institute on Aging grants totaling $747,250. The first grant, funded at $374,850, investigated the role of glucose transport in Alzheimer's disease pathogenesis. The second grant, funded at $372,400, examined the compromised function of a glial glucose transporter in aging and Alzheimer's disease.
His recent publications explore various molecular and cellular mechanisms implicated in neurodegeneration. These include studies on lysosomal autophagic failure in Alzheimer's disease, the role of serine racemase expression in differentiating aging from Alzheimer's brains, and the inhibition of aggregation-mediated pathology by thiadiazolidinone analogs in diverse neurodegeneration models. Dr. Barger also investigates novel system xC− transport inhibitors to mitigate microglial glutamate release and neurotoxicity, and the effects of reelin fragments on cognitive deficits in mouse models. Further research includes examining endoplasmic reticulum stress in hypothalamic neurons and the association of P-glycoprotein substrates with Alzheimer's disease risk.
Dr. Barger collaborates with researchers from the University of Arkansas at Little Rock and within the University of Arkansas for Medical Sciences. His work has resulted in 147 publications, with 10,294 citations, and he holds an h-index of 49.
Metrics
- h-index: 49
- Publications: 142
- Citations: 10,302
Selected Publications
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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)
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Serine Racemase Expression Differentiates Aging from Alzheimer’s Brain (2022)
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Amyloid β-peptide impacts on glucose regulation are dependent on apolipoprotein E genotype (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
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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