Meenakshisundaram Balasubramaniam Institution-verified
Sourced from institutional research profiles (UAMS TRI or ARA).
Assistant Professor
faculty
Research Areas
Biography and Research Information
OverviewAI-generated summary
Meenakshisundaram Balasubramaniam's research focuses on understanding the molecular mechanisms underlying neurodegenerative diseases, particularly Alzheimer's disease and glioblastoma. His work investigates the role of protein aggregates, including glial fibrillary acidic protein (GFAP), as potential biomarkers for neurodegeneration. Balasubramaniam also explores the therapeutic potential of small molecules, such as novel hydroxybenzylamine-deoxyvasicinone hybrids and compounds that can rescue lysosomal autophagic failure, in treating Alzheimer's disease. His research extends to the broader implications of protein aggregation in age-associated diseases, including myocardial infarction, and the role of mitochondria in aging.
Balasubramaniam has published on topics including the identification of intrinsically disordered proteins in the aggregate proteome, the composition of protein aggregates with RNA and DNA, and the potential of epidermal growth factor receptor inhibitors in glioblastoma treatment. He leads a research group and collaborates with several colleagues at the University of Arkansas for Medical Sciences, including Srinivas Ayyadevara, Robert J. Shmookler Reis, Akshatha Ganne, and W. Sue T. Griffin, with whom he has co-authored numerous publications.
His scholarship metrics include an h-index of 22, with 55 total publications and 1,216 total citations. He is recognized as a highly cited researcher.
Metrics
- h-index: 22
- Publications: 56
- Citations: 1,246
Selected Publications
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Zolpidem restores sleep and decreases amyloid in a mouse model (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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Zolpidem restores sleep and slows Alzheimer’s progression in a mouse model (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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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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Mitochondria in aging and age-associated diseases (2025)
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Metabolomic Profiling and Machine Learning Models for Tumor Classification in Patients with Recurrent IDH-Wild-Type Glioblastoma: A Prospective Study (2024)
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Tools of Artificial Intelligence in the Improvement of Synaptic Impairment in Different Neurodegenerative Diseases (2024)
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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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Epidermal Growth Factor Receptor Inhibitors in Glioblastoma: Current Status and Future Possibilities (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)
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 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
- 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 15 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 15 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
- Alzheimer’s-specific brain amyloid interactome: Neural-network analysis of intra-aggregate crosslinking identifies novel drug targets
Showing 5 of 7 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
- Alzheimer’s-specific brain amyloid interactome: Neural-network analysis of intra-aggregate crosslinking identifies novel drug targets
- Ezetimibe Lowers Risk of Alzheimer’s and Related Dementias over Sevenfold, Reducing Aggregation in Model Systems by Inhibiting 14-3-3G::Hexokinase Interaction
- Tools of Artificial Intelligence in the Improvement of Synaptic Impairment in Different Neurodegenerative Diseases
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer’s-like neuropathology
Showing 5 of 6 shared publications
- “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
- 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
- Epidermal Growth Factor Receptor Inhibitors in Glioblastoma: Current Status and Future Possibilities
- 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
- Metabolomic Profiling and Machine Learning Models for Tumor Classification in Patients with Recurrent IDH-Wild-Type Glioblastoma: A Prospective Study
- 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
- Novel hydroxybenzylamine-deoxyvasicinone hybrids as anticholinesterase therapeutics for Alzheimer’s disease
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Antitumor properties of novel sesquiterpene lactone analogs as NFκB inhibitors that bind to the IKKβ ubiquitin-like domain (ULD)
- Novel hydroxybenzylamine-deoxyvasicinone hybrids as anticholinesterase therapeutics for Alzheimer’s disease
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Antitumor properties of novel sesquiterpene lactone analogs as NFκB inhibitors that bind to the IKKβ ubiquitin-like domain (ULD)
- Rescue of ApoE4-related lysosomal autophagic failure in Alzheimer’s disease by targeted small molecules
- In silico analysis of TUBA4A mutations in Amyotrophic Lateral Sclerosis to define mechanisms of microtubule disintegration
- In Silico Analysis of TUBA4A Mutations in Amyotrophic Lateral Sclerosis to Define Mechanisms of Microtubule Disintegration
- In silico analysis of TUBA4A mutations in Amyotrophic Lateral Sclerosis to define mechanisms of microtubule disintegration
- In Silico Analysis of TUBA4A Mutations in Amyotrophic Lateral Sclerosis to Define Mechanisms of Microtubule Disintegration
- In silico analysis of TUBA4A mutations in Amyotrophic Lateral Sclerosis to define mechanisms of microtubule disintegration
- In Silico Analysis of TUBA4A Mutations in Amyotrophic Lateral Sclerosis to Define Mechanisms of Microtubule Disintegration
- In silico analysis of TUBA4A mutations in Amyotrophic Lateral Sclerosis to define mechanisms of microtubule disintegration
- In Silico Analysis of TUBA4A Mutations in Amyotrophic Lateral Sclerosis to Define Mechanisms of Microtubule Disintegration
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