W. Sue T. Griffin
Professor
faculty
Geriatrics, College of Medicine
Research Areas
Biography and Research Information
OverviewAI-generated summary
W. Sue T. Griffin's research investigates the molecular mechanisms underlying neurodegenerative diseases, with a significant focus on Alzheimer's disease and glioblastoma. Her work explores the roles of specific proteins, cytokines, and microbial factors in disease pathogenesis and potential therapeutic targets. Griffin has published research on the involvement of Porphyromonas gingivalis outer membrane vesicles in Alzheimer's neuropathogenesis, the impact of APOEε4 genetics and neuroinflammation on Alzheimer's disease, and the potential of thiadiazolidinone (TDZD) analogs to inhibit aggregation-related pathology in neurodegeneration models. She also studies the role of the proinflammatory cytokine IL-1β in glioblastoma, examining the therapeutic effects of IL-1β receptor antagonist and Tolcapone. Her recent work also delves into lysosomal autophagic failure in Alzheimer's disease and the potential for small molecule rescue, as well as the role of glial fibrillary acidic protein as a biomarker and drug target for Alzheimer's disease. Further investigations include the proteome of Caenorhabditis elegans mitochondria in relation to aging and Alzheimer's disease.
Metrics
- h-index: 66
- Publications: 173
- Citations: 17,510
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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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)
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
- 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
- Neuroinflammation, Protein Aggregates, ApoE4 Drug Targeting, and Autophagy Rescue NIH/Nat. Inst. on Aging 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
Collaboration Network
Top Collaborators
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- 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
- When Two Worlds Collide: The Contribution and Association Between Genetics (APOEε4) and Neuroinflammation (IL-1β) in Alzheimer’s Neuropathogenesis
Showing 5 of 6 shared publications
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- 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
- When Two Worlds Collide: The Contribution and Association Between Genetics (APOEε4) and Neuroinflammation (IL-1β) in Alzheimer’s Neuropathogenesis
Showing 5 of 6 shared publications
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- 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
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer's Disease
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- 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
- 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
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
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