W. Sue T. Griffin
Professor
Also affiliated: Northwestern University (1996); National Institutes of Health (1987); Arkansas Children's Hospital (1993–1999); United States Department of Veterans Affairs (1995–2003); Uniformed Services University of the Health Sciences (1987); The University of Texas at Dallas (1978–1986); The University of Texas System (1981); Eli Lilly (United States) (2000); University of Arkansas Medical Center (1995–2015); Veterans Health Administration (1996–2003); Ruijin Hospital (1995–1996); University of Rochester Medicine (1975); University of the Ryukyus (1996); University of Texas Health Science Center at Dallas (1977–1987); Central Arkansas Veterans Healthcare System (1995–2025); Geriatric Research Education and Clinical Center (1997–2008); National Institute of Neurological Disorders and Stroke (1987); Mental Illness Research, Education and Clinical Centers (2000); John L. McClellan Memorial Veterans Hospital (1997–2016); Indiana University School of Medicine (2000); Arkansas Children's Research Institute (1996–1999); University of Rochester (1975); Weizmann Institute of Science (1989); New York University (1992); The University of Texas Southwestern Medical Center (1975–1985)
Geriatrics, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
W. Sue T. Griffin investigates the complex interplay of neuroinflammation and neurodegeneration, with a particular focus on Alzheimer's disease. Her research group explores the role of glial cells, such as microglia, and their secreted cytokines in the progression of neurodegenerative processes. Griffin's work has examined the expression of interleukin-1 in different plaque types within Alzheimer's disease brains and investigated how this cytokine mediates pathological effects on neurons through specific signaling pathways like p38-MAPK. Her studies also extend to the broader context of neuroinflammation, including its presence in conditions like Down syndrome.
Griffin has secured federal funding for her research, including a $470,331 grant from the NIH/National Institute on Aging. This project focuses on neuroinflammation, protein aggregates, ApoE4 drug targeting, and autophagy rescue. Her extensive publication record includes over 170 articles, and she is recognized as a highly cited researcher with an h-index of 66. Griffin actively collaborates with colleagues at the University of Arkansas for Medical Sciences, including Srinivas Ayyadevara and Meenakshisundaram Balasubramaniam, on multiple shared publications, contributing to a robust research network.
Metrics
- h-index: 66
- Publications: 170
- Citations: 17,693
Positions
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Professor publications 1989–2026University of Arkansas for Medical Sciences Geriatrics, College of Medicine Institutional directory
Selected Publications
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Abstract LB320: Inverse relationship between cancer and Alzheimer’s disease: Important interplay between autophagy and apoptosis signaling mechanisms (2026)
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The aggregate proteome of Caenorhabditis elegans mitochondria implicates shared mechanisms of aging and Alzheimer’s disease (2026)
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When Two Worlds Collide: The Contribution and Association Between Genetics (APOEε4) and Neuroinflammation (IL-1β) in Alzheimer’s Neuropathogenesis (2025)
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The Seminal Role of the Proinflammatory Cytokine IL-1β and Its Signaling Cascade in Glioblastoma Pathogenesis and the Therapeutic Effect of Interleukin-1β Receptor Antagonist (IL-1RA) and Tolcapone (2025)
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Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer’s-like neuropathology (2025)
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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)
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Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules (2024)
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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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Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease (2022)
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Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer's Disease (2021)
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Porphyromonas gingivalis Outer Membrane Vesicles as the Major Driver of and Explanation for Neuropathogenesis, the Cholinergic Hypothesis, Iron Dyshomeostasis, and Salivary Lactoferrin in Alzheimer’s Disease (2021)
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Interleukin-1β drives NEDD8 nuclear-to-cytoplasmic translocation, fostering parkin activation via NEDD8 binding to the P-ubiquitin activating site (2019)
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A Novel Microtubule-Binding Drug Attenuates and Reverses Protein Aggregation in Animal Models of Alzheimer’s Disease (2019)
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Aggregate Interactome Based on Protein Cross-linking Interfaces Predicts Drug Targets to Limit Aggregation in Neurodegenerative Diseases (2019)
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P2‐181: IL‐1β INFLUENCES AUTOPHAGY BY MEDIATING UPREGULATION OF PARKIN AND PARKIN NEDDYLATION IN CELL CULTURE AND ANIMAL MODELS, AND MIMICS THE PATTERN SEEN IN AD BRAIN (2018)
Federal Grants 2 $1,058,437 total
Neuroinflammation, Protein Aggregates, ApoE4 Drug Targeting, and Autophagy Rescue
The Protein C Pathway in Mitigation of Radiation-Induced Endothelial and Vascular Dysfunction
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- GENE EXPRESSION IN BRAIN CELLS IN AIDS NIH Principal Investigator
- Early Events in Alzheimer Pathogenesis NIH Principal Investigator
- CYTOKINES, NEURODEGENERATION AND DOWN'S SYNDROME NIH Principal Investigator
- BRAIN DEVELOPMENT AND GRAFT VERSUS HOST DISEASE NIH Principal Investigator
- Compromised function of a glial glucose transporter in aging and Alzheimer's disease NIH Co-Investigator
- Amyloid Precursor Protein and Ubiquitination NIH/Nat. Inst. on Aging Co-Investigator
- Center for Translational Neuroscience NIH Co-Investigator
- ALTERED GENE EXPRESSION IN ALZHEIMER SENILE DEMENTIA NIH Principal Investigator
Collaboration Network
Top Collaborators
- Microglia and neuroinflammation: a pathological perspective.
- Glial‐Neuronal Interactions in Alzheimer's Disease: The Potential Role of a ‘Cytokine Cycle’ in Disease Progression
- Glia and their cytokines in progression of neurodegeneration
- Glial cytokines in Alzheimer's disease: Review and pathogenic implications
- Association of interleukin-1 gene polymorphisms with Alzheimer's disease
Showing 5 of 52 shared publications
- Glial‐Neuronal Interactions in Alzheimer's Disease: The Potential Role of a ‘Cytokine Cycle’ in Disease Progression
- Interleukin-1 Expression in Different Plaque Types in Alzheimerʼs Disease
- Glial cytokines in Alzheimer's disease: Review and pathogenic implications
- In vivo and in vitro evidence supporting a role for the inflammatory cytokine interleukin-1 as a driving force in Alzheimer pathogenesis
- Alterations in synaptic proteins and their encoding mRNAs in prefrontal cortex in schizophrenia: a possible neurochemical basis for ‘hypofrontality’
Showing 5 of 22 shared publications
- Interleukin-1 Mediates Pathological Effects of Microglia on Tau Phosphorylation and on Synaptophysin Synthesis in Cortical Neurons through a p38-MAPK Pathway
- Interleukin-1 mediates Alzheimer and Lewy body pathologies
- Neuronal–Glial Interactions Mediated by Interleukin-1 Enhance Neuronal Acetylcholinesterase Activity and mRNA Expression
- Induction of serine racemase expression and D-serine release from microglia by amyloid beta-peptide.
- Vitamin E suppression of microglial activation is neuroprotective
Showing 5 of 17 shared publications
- Apolipoprotein E4 inhibits autophagy gene products through direct, specific binding to CLEAR motifs
- Proteins that mediate protein aggregation and cytotoxicity distinguish Alzheimer's hippocampus from normal controls
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Interleukin-1β drives NEDD8 nuclear-to-cytoplasmic translocation, fostering parkin activation via NEDD8 binding to the P-ubiquitin activating site
- Aggregate Interactome Based on Protein Cross-linking Interfaces Predicts Drug Targets to Limit Aggregation in Neurodegenerative Diseases
Showing 5 of 16 shared publications
- Apolipoprotein E4 inhibits autophagy gene products through direct, specific binding to CLEAR motifs
- Proteins that mediate protein aggregation and cytotoxicity distinguish Alzheimer's hippocampus from normal controls
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Aggregate Interactome Based on Protein Cross-linking Interfaces Predicts Drug Targets to Limit Aggregation in Neurodegenerative Diseases
- A Novel Microtubule-Binding Drug Attenuates and Reverses Protein Aggregation in Animal Models of Alzheimer’s Disease
Showing 5 of 14 shared publications
- Interleukin-1 promotion of MAPK-p38 overexpression in experimental animals and in Alzheimer's disease: potential significance for tau protein phosphorylation
- Interleukin-1 Promotes Expression and Phosphorylation of Neurofilament and tau Proteins in Vivo
- Apolipoprotein E4 inhibits autophagy gene products through direct, specific binding to CLEAR motifs
- S100β Increases Levels of β‐Amyloid Precursor Protein and Its Encoding mRNA in Rat Neuronal Cultures
- Overexpression of the Neuritotrophic Cytokine S100β Precedes the Appearance of Neuritic β‐Amyloid Plaques in APPV717F Mice
Showing 5 of 10 shared publications
- In vivo and in vitro evidence supporting a role for the inflammatory cytokine interleukin-1 as a driving force in Alzheimer pathogenesis
- S100β expression in Alzheimer's disease: Relation to neuropathology in brain regions
- Interleukin-1 promotion of MAPK-p38 overexpression in experimental animals and in Alzheimer's disease: potential significance for tau protein phosphorylation
- Human brain S100β and S100β mRNA expression increases with age: Pathogenic implications for Alzheimer's disease
- Overexpression of the Neurotrophic Cytokine S100β in Human Temporal Lobe Epilepsy
Showing 5 of 9 shared publications
- Apolipoprotein E4 inhibits autophagy gene products through direct, specific binding to CLEAR motifs
- Proteins that mediate protein aggregation and cytotoxicity distinguish Alzheimer's hippocampus from normal controls
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Aggregate Interactome Based on Protein Cross-linking Interfaces Predicts Drug Targets to Limit Aggregation in Neurodegenerative Diseases
- A Novel Microtubule-Binding Drug Attenuates and Reverses Protein Aggregation in Animal Models of Alzheimer’s Disease
Showing 5 of 9 shared publications
- Interleukin-1 Mediates Pathological Effects of Microglia on Tau Phosphorylation and on Synaptophysin Synthesis in Cortical Neurons through a p38-MAPK Pathway
- Interleukin-1 mediates Alzheimer and Lewy body pathologies
- Vitamin E suppression of microglial activation is neuroprotective
- S100β Increases Levels of β‐Amyloid Precursor Protein and Its Encoding mRNA in Rat Neuronal Cultures
- S100B‐induced microglial and neuronal IL‐1 expression is mediated by cell type‐specific transcription factors
Showing 5 of 7 shared publications
- Alterations in synaptic proteins and their encoding mRNAs in prefrontal cortex in schizophrenia: a possible neurochemical basis for ‘hypofrontality’
- Mitogen-activated protein kinases in schizophrenia
- Nitric oxide synthase (NOS) in schizophrenia
- Decreased mesopontine choline acetyltransferase levels in schizophrenia
- In vitro 1H-magnetic resonance spectroscopy of postmortem brains with schizophrenia
Showing 5 of 7 shared publications
- Interleukin-1 Mediates Pathological Effects of Microglia on Tau Phosphorylation and on Synaptophysin Synthesis in Cortical Neurons through a p38-MAPK Pathway
- S100β Induction of the Proinflammatory Cytokine Interleukin‐6 in Neurons
- S100B‐induced microglial and neuronal IL‐1 expression is mediated by cell type‐specific transcription factors
- Aging, Alzheimer's, and APOE genotype influence the expression and neuronal distribution patterns of microtubule motor protein dynactin-P50
- Microglial activation by uptake of fDNA via a scavenger receptor
Showing 5 of 7 shared publications
- Glial‐Neuronal Interactions in Alzheimer's Disease: The Potential Role of a ‘Cytokine Cycle’ in Disease Progression
- Association of interleukin-1 gene polymorphisms with Alzheimer's disease
- Long-term intracerebral inflammatory response after traumatic brain injury
- Aging-associated Changes in Human Brain
- The neuroinflammatory response in humans after traumatic brain injury
Showing 5 of 7 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
- The Seminal Role of the Proinflammatory Cytokine IL-1β and Its Signaling Cascade in Glioblastoma Pathogenesis and the Therapeutic Effect of Interleukin-1β Receptor Antagonist (IL-1RA) and Tolcapone
Showing 5 of 6 shared publications
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Aggregate Interactome Based on Protein Cross-linking Interfaces Predicts Drug Targets to Limit Aggregation in Neurodegenerative Diseases
- A Novel Microtubule-Binding Drug Attenuates and Reverses Protein Aggregation in Animal Models of Alzheimer’s Disease
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- The aggregate proteome of Caenorhabditis elegans mitochondria implicates shared mechanisms of aging and Alzheimer’s disease
Showing 5 of 6 shared publications
- Interleukin-1 Expression in Different Plaque Types in Alzheimerʼs Disease
- Neuronal–Glial Interactions Mediated by Interleukin-1 Enhance Neuronal Acetylcholinesterase Activity and mRNA Expression
- Human brain S100β and S100β mRNA expression increases with age: Pathogenic implications for Alzheimer's disease
- S100β Induction of the Proinflammatory Cytokine Interleukin‐6 in Neurons
- Progressive Neuronal Injury Associated with Amyloid Plaque Formation in Alzheimer Disease
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