Nirjal Mainali
Researcher
Also affiliated: Institute on Aging (2023–2025)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Nirjal Mainali investigates the molecular mechanisms underlying aging and age-associated neurodegenerative diseases, with a particular focus on the roles of mitochondria and endoplasmic reticulum stress. His research explores how cellular dysfunction contributes to conditions such as Alzheimer's disease and myocardial infarction. Mainali's work has identified potential therapeutic strategies, including the inhibition of protein aggregation and the targeting of specific protein interactions, such as the 14-3-3G::Hexokinase interaction. He has also developed computational tools, like the leave-one-out-analysis (LOOA) web-based tool, to aid in the analysis of proteomic data related to aggregate crosslinking. Mainali has a significant publication record, with a recent emphasis on Alzheimer's disease and related dementias, and collaborates extensively with researchers at the University of Arkansas for Medical Sciences, including Robert J. Shmookler Reis and Srinivas Ayyadevara.
Metrics
- h-index: 8
- Publications: 14
- Citations: 191
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
- 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 9 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 9 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 6 shared publications
- Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain
- 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
- 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
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer’s-like neuropathology
- 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
- Physiological Consequences of Targeting 14-3-3 and Its Interacting Partners in Neurodegenerative Diseases
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
- Thiadiazolidinone (TDZD) Analogs Inhibit Aggregation-Mediated Pathology in Diverse Neurodegeneration Models, and Extend C. elegans Life- and Healthspan
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