Biography and Research Information
OverviewAI-generated summary
Nirjal Mainali's research investigates the role of mitochondria and endoplasmic reticulum stress in aging and age-associated neurodegenerative diseases. His work has explored how these cellular processes contribute to protein aggregation and pathology in conditions such as Alzheimer's disease and myocardial infarction. Mainali has studied the potential of pharmacological interventions, including thiadiazolidinone analogs and ezetimibe, to inhibit aggregation-mediated pathology and extend healthspan in model organisms like *C. elegans*. He has also focused on identifying novel drug targets by analyzing the brain amyloid interactome and developing computational tools for proteomic data analysis. Mainali collaborates with researchers at the University of Arkansas for Medical Sciences, including Robert J. Shmookler Reis and Srinivas Ayyadevara, with whom he has co-authored multiple publications. His scholarship metrics include an h-index of 8, with 13 total publications and 165 citations.
Metrics
- h-index: 8
- Publications: 14
- Citations: 181
Selected Publications
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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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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)
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 10 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
- 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 7 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
- 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
- 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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