W. Sue T. Griffin
Professor
Also affiliated: Northwestern University (1996); Google (United States) (1982); National Institutes of Health (1987); Arkansas Children's Hospital (1993–1999); United States Department of Veterans Affairs (1997–1998); Uniformed Services University of the Health Sciences (1987); The University of Texas at Dallas (1986); Eli Lilly (United States) (2000); British Geriatrics Society (1998); University of Arkansas Medical Center (1996–2024); Arkansas Department of Education (2000); Veterans Health Administration (1996–2002); St. Boniface Hospital (1981); Pamela Youde Nethersole Eastern Hospital (2016); University of the Ryukyus (1996); Stephens College (2013); University of Texas Health Science Center at Dallas (1977–1987); Central Arkansas Veterans Healthcare System (1996–2025); Geriatric Research Education and Clinical Center (1997–2019); National Institute of Neurological Disorders and Stroke (1987); Mental Illness Research, Education and Clinical Centers (2000–2003); Geospatial Research (United Kingdom) (2025); Institute on Aging (2009–2025); National Cancer Institute (1969); Pediatrics and Genetics (1995); John L. McClellan Memorial Veterans Hospital (1997–2000); Arkansas Department of Agriculture (1989–2014); Southwestern Medical Center (1975–1981); University of Rochester (1975); Weizmann Institute of Science (1989); Indiana University – Purdue University Indianapolis (2000); New York University (1992); University of Pennsylvania (2025); The University of Texas Southwestern Medical Center (1975–1985); U.S. Army Engineer Research and Development Center (2025); The University of Texas Health Science Center at Houston (1977–1981); Philadelphia University (2025)
Faculty Researcher
Geriatrics, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
W. Sue T. Griffin's research investigates the mechanisms underlying neurodegenerative diseases, with a particular focus on Alzheimer's disease and glioblastoma. Griffin's work explores the roles of specific biological factors, such as the proinflammatory cytokine IL-1β, glial fibrillary acidic protein (GFAP), and the APOEε4 genotype, in disease pathogenesis. She has published research examining how Porphyromonas gingivalis outer membrane vesicles contribute to Alzheimer's neuropathogenesis, including its effects on the cholinergic hypothesis and iron dyshomeostasis. Additionally, her research has identified GFAP as a potential biomarker and therapeutic target for Alzheimer's disease and investigated the use of thiadiazolidinone (TDZD) analogs to inhibit aggregation-related pathology in neurodegeneration models.
Metrics
- h-index: 66
- Publications: 172
- Citations: 17,643
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 1 $470,331 total
Neuroinflammation, Protein Aggregates, ApoE4 Drug Targeting, and Autophagy Rescue
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
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- 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
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer's Disease
- 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
Showing 5 of 9 shared publications
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- 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
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer's Disease
- 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
Showing 5 of 8 shared publications
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer's Disease
- The aggregate proteome of Caenorhabditis elegans mitochondria implicates shared mechanisms of aging and Alzheimer’s disease
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer’s-like neuropathology
- 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
- 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
- When Two Worlds Collide: The Contribution and Association Between Genetics (APOEε4) and Neuroinflammation (IL-1β) in Alzheimer’s Neuropathogenesis
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer’s-like neuropathology
- 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
- 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
- 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
- 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
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer’s-like neuropathology
- The aggregate proteome of Caenorhabditis elegans mitochondria implicates shared mechanisms of aging and Alzheimer’s disease
- 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
- 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
- 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
- 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
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer's Disease
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
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