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Biography and Research Information
OverviewAI-generated summary
Nirjal Mainali's research focuses on neurodegenerative diseases, aging, and the development of therapeutic strategies. His work investigates the molecular mechanisms underlying conditions such as Alzheimer's disease and other age-associated neurodegenerative disorders. Mainali has explored the role of cellular processes like endoplasmic reticulum stress and mitochondrial function in aging and disease pathogenesis. He also studies the aggregation of proteins, such as amyloid-beta, and has investigated compounds that can inhibit this aggregation or chelate metals implicated in disease progression.
His research has involved both animal models, including mice and *C. elegans*, and computational approaches like structural modeling of key enzymes such as GSK3β. Mainali has published on the physiological consequences of targeting specific cellular pathways and interactions, and has explored the potential of existing drugs, like Ezetimibe, for new therapeutic applications in neurodegeneration. His work is supported by collaborations with researchers at the University of Arkansas for Medical Sciences, including Robert J. Shmookler Reis and Srinivas Ayyadevara.
Metrics
- h-index: 9
- Publications: 14
- Citations: 198
Positions
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Post Doctoral Fellow 2025–presentUniversity of Arkansas for Medical Sciences Geriatrics ORCID
Selected Publications
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Development of an AI-Enhanced Workflow for Automated Quality Classification of Biomedical Fluorescence (2026)
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Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer’s-like neuropathology (2025)
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Mitochondria in aging and age-associated diseases (2025)
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Strong reduction of cryoprotectant toxicity by stress response induction (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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Model biological systems demonstrate the inducibility of pathways that strongly reduce cryoprotectant toxicity (2024)
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Leave-one-out-analysis (LOOA): web-based tool to predict influential proteins and interactions in aggregate-crosslinking proteomic data (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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Protein homeostasis in the aged and diseased heart (2023)
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Physiological Consequences of Targeting 14-3-3 and Its Interacting Partners in Neurodegenerative Diseases (2022)
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Structural modeling of GSK3β implicates the inactive (DFG-out) conformation as the target bound by TDZD analogs (2020)
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Design and Synthesis of Novel Hybrid 8-Hydroxy Quinoline-Indole Derivatives as Inhibitors of Aβ Self-Aggregation and Metal Chelation-Induced Aβ Aggregation (2020)
Collaboration Network
Top Collaborators
- Design and Synthesis of Novel Hybrid 8-Hydroxy Quinoline-Indole Derivatives as Inhibitors of Aβ Self-Aggregation and Metal Chelation-Induced Aβ Aggregation
- 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
- 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 12 shared publications
- Structural modeling of GSK3β implicates the inactive (DFG-out) conformation as the target bound by TDZD analogs
- Design and Synthesis of Novel Hybrid 8-Hydroxy Quinoline-Indole Derivatives as Inhibitors of Aβ Self-Aggregation and Metal Chelation-Induced Aβ Aggregation
- 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
Showing 5 of 12 shared publications
- Structural modeling of GSK3β implicates the inactive (DFG-out) conformation as the target bound by TDZD analogs
- 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
- 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 8 shared publications
- Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain
- Ezetimibe Lowers Risk of Alzheimer’s and Related Dementias over Sevenfold, Reducing Aggregation in Model Systems by Inhibiting 14-3-3G::Hexokinase Interaction
- 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
- Protein homeostasis in the aged and diseased heart
- 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
- Structural modeling of GSK3β implicates the inactive (DFG-out) conformation as the target bound by TDZD analogs
- Design and Synthesis of Novel Hybrid 8-Hydroxy Quinoline-Indole Derivatives as Inhibitors of Aβ Self-Aggregation and Metal Chelation-Induced Aβ Aggregation
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Design and Synthesis of Novel Hybrid 8-Hydroxy Quinoline-Indole Derivatives as Inhibitors of Aβ Self-Aggregation and Metal Chelation-Induced Aβ Aggregation
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Development of an AI-Enhanced Workflow for Automated Quality Classification of Biomedical Fluorescence
- Structural modeling of GSK3β implicates the inactive (DFG-out) conformation as the target bound by TDZD analogs
- Design and Synthesis of Novel Hybrid 8-Hydroxy Quinoline-Indole Derivatives as Inhibitors of Aβ Self-Aggregation and Metal Chelation-Induced Aβ Aggregation
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Structural modeling of GSK3β implicates the inactive (DFG-out) conformation as the target bound by TDZD analogs
- Physiological Consequences of Targeting 14-3-3 and Its Interacting Partners in Neurodegenerative Diseases
- Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain
- Protein homeostasis in the aged and diseased heart
- 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
- Model biological systems demonstrate the inducibility of pathways that strongly reduce cryoprotectant toxicity
- Strong reduction of cryoprotectant toxicity by stress response induction
- Model biological systems demonstrate the inducibility of pathways that strongly reduce cryoprotectant toxicity
- Strong reduction of cryoprotectant toxicity by stress response induction
- Model biological systems demonstrate the inducibility of pathways that strongly reduce cryoprotectant toxicity
- Strong reduction of cryoprotectant toxicity by stress response induction
- Model biological systems demonstrate the inducibility of pathways that strongly reduce cryoprotectant toxicity
- Strong reduction of cryoprotectant toxicity by stress response induction
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