Srinivas Ayyadevara Institution-verified
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Biography and Research Information
OverviewAI-generated summary
Srinivas Ayyadevara's research focuses on understanding the molecular mechanisms underlying aging and age-associated neurodegenerative diseases. His work investigates the role of protein aggregation, intrinsically disordered proteins, and mitochondrial dysfunction in these processes. Ayyadevara has explored potential therapeutic strategies, including the development of novel anticholinesterase agents and small molecules to address lysosomal autophagic failure in Alzheimer's disease.
His research has been supported by federal grants, including an NIH/National Institute on Aging award totaling $374,971 for investigating common pathways in neurodegeneration and other age-progressive diseases. Ayyadevara collaborates with several researchers at the University of Arkansas for Medical Sciences, including Robert J. Shmookler Reis, Meenakshisundaram Balasubramaniam, Akshatha Ganne, and Nirjal Mainali, with whom he has co-authored numerous publications.
Ayyadevara's publication record includes studies on glial fibrillary acidic protein as a biomarker for Alzheimer's disease, the role of RNA and DNA within protein aggregates, and the impact of myocardial infarction on protein aggregation in both the heart and brain. His work also utilizes machine learning to identify factors contributing to neurodegeneration. He has a h-index of 30 with over 5,195 citations across 89 publications, and is recognized as a highly cited researcher.
Metrics
- h-index: 31
- Publications: 91
- Citations: 5,332
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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Machine Learning–Enhanced Quantitative Structure-Activity Relationship Modeling for DNA Polymerase Inhibitor Discovery: Algorithm Development and Validation (2025)
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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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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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Mitochondria in aging and age-associated diseases (2025)
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Ezetimibe Lowers Risk of Alzheimer’s and Related Dementias over Sevenfold, Reducing Aggregation in Model Systems by Inhibiting 14-3-3G::Hexokinase Interaction (2024)
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Model biological systems demonstrate the inducibility of pathways that strongly reduce cryoprotectant toxicity (2024)
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Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules (2024)
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Alzheimer’s-specific brain amyloid interactome: Neural-network analysis of intra-aggregate crosslinking identifies novel drug targets (2023)
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Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain (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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Proteomic analysis of transcription factors involved in the alteration of ischemic mouse heart as modulated by MSC exosomes (2023)
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Proteomic Analysis of Transcription Factors Involved in the Alteration of Ischemic Mouse Heart as Modulated by MSC Exosomes (2023)
Federal Grants 1 $374,971 total
Inference of Common Pathways Underlying Neurodegeneration & Other Age-Progressive Diseases
Grants & Funding
Collaboration Network
Top Collaborators
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Intrinsically disordered proteins identified in the aggregate proteome serve as biomarkers of neurodegeneration
- “Protein aggregates” contain RNA and DNA, entrapped by misfolded proteins but largely rescued by slowing translational elongation
- Novel hydroxybenzylamine-deoxyvasicinone hybrids as anticholinesterase therapeutics for Alzheimer’s disease
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
Showing 5 of 28 shared publications
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Intrinsically disordered proteins identified in the aggregate proteome serve as biomarkers of neurodegeneration
- “Protein aggregates” contain RNA and DNA, entrapped by misfolded proteins but largely rescued by slowing translational elongation
- Novel hydroxybenzylamine-deoxyvasicinone hybrids as anticholinesterase therapeutics for Alzheimer’s disease
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
Showing 5 of 18 shared publications
- Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease
- Intrinsically disordered proteins identified in the aggregate proteome serve as biomarkers of neurodegeneration
- “Protein aggregates” contain RNA and DNA, entrapped by misfolded proteins but largely rescued by slowing translational elongation
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain
Showing 5 of 12 shared publications
- Mitochondria in aging and age-associated diseases
- Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Physiological Consequences of Targeting 14-3-3 and Its Interacting Partners in Neurodegenerative Diseases
- Ezetimibe Lowers Risk of Alzheimer’s and Related Dementias over Sevenfold, Reducing Aggregation in Model Systems by Inhibiting 14-3-3G::Hexokinase Interaction
Showing 5 of 10 shared publications
- Supplementary Figure 3: Dinaciclib reduces the mRNA transcripts of Rad51, its paralogs and Brca1 in vivo from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
Showing 5 of 8 shared publications
- Supplementary Figure 3: Dinaciclib reduces the mRNA transcripts of Rad51, its paralogs and Brca1 in vivo from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
Showing 5 of 8 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
- Mitochondria in aging and age-associated diseases
- Ezetimibe Lowers Risk of Alzheimer’s and Related Dementias over Sevenfold, Reducing Aggregation in Model Systems by Inhibiting 14-3-3G::Hexokinase Interaction
- Alzheimer’s-specific brain amyloid interactome: Neural-network analysis of intra-aggregate crosslinking identifies novel drug targets
- 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
- “Protein aggregates” contain RNA and DNA, entrapped by misfolded proteins but largely rescued by slowing translational elongation
- 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
- Ezetimibe Lowers Risk of Alzheimer’s and Related Dementias over Sevenfold, Reducing Aggregation in Model Systems by Inhibiting 14-3-3G::Hexokinase Interaction
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- DNA Polymerase Inhibitor Discovery Using Machine Learning-Enhanced QSAR Modeling
- Advanced QSAR Modeling with Machine Learning for Drug Discovery: Targeting DNA Polymerase Inhibitors. (Preprint)
- Machine Learning–Enhanced Quantitative Structure-Activity Relationship Modeling for DNA Polymerase Inhibitor Discovery: Algorithm Development and Validation
- 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
- Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain
- Protein homeostasis in the aged and diseased heart
- Proteomic analysis of transcription factors involved in the alteration of ischemic mouse heart as modulated by MSC exosomes
- Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain
- Proteomic Analysis of Transcription Factors Involved in the Alteration of Ischemic Mouse Heart as Modulated by MSC Exosomes
- Proteomic analysis of transcription factors involved in the alteration of ischemic mouse heart as modulated by MSC exosomes
- DNA Polymerase Inhibitor Discovery Using Machine Learning-Enhanced QSAR Modeling
- Advanced QSAR Modeling with Machine Learning for Drug Discovery: Targeting DNA Polymerase Inhibitors. (Preprint)
- Machine Learning–Enhanced Quantitative Structure-Activity Relationship Modeling for DNA Polymerase Inhibitor Discovery: Algorithm Development and Validation
- DNA Polymerase Inhibitor Discovery Using Machine Learning-Enhanced QSAR Modeling
- Advanced QSAR Modeling with Machine Learning for Drug Discovery: Targeting DNA Polymerase Inhibitors. (Preprint)
- Machine Learning–Enhanced Quantitative Structure-Activity Relationship Modeling for DNA Polymerase Inhibitor Discovery: Algorithm Development and Validation
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