Gerald A. Dienel
High Impact
UAMS Contingent Worker
faculty
Neurology, College of Medicine
48 h-index
150 pubs
10,617 cited
Research Areas
Biography and Research Information
OverviewAI-generated summary
Gerald A. Dienel's research focuses on brain energy metabolism, particularly investigating the mechanisms underlying neuronal glucose oxidation and its relationship with neurotransmission. His work explores how astrocytes and neurons utilize glucose and glycogen to maintain brain homeostasis during activation, examining the role of nonoxidative glycolysis in compensating for increased proton production and influencing neuroimaging signals like the BOLD response.
Dienel has also studied potential roles for glycogen in epilepsy and investigated metabolic reprogramming in neurons associated with familial ALS. His research group investigates artifacts that can occur during brain tissue harvesting, developing methods to prevent enzyme inactivation and ensure accurate metabolic measurements. With a h-index of 47 and over 10,500 citations, Dienel is recognized as a highly cited researcher in his field.
Metrics
- h-index: 48
- Publications: 150
- Citations: 10,617
Selected Publications
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Reply to Comment by Quistorff: ATP is not consumed solely by hydrolytic reactions (2025)
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Revisiting phenylketonuria: Do high brain glycine levels caused by chronic hyperphenylalanemia contribute to brain dysfunction by modulating D-serine levels and NMDA receptor activity? (2025)
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Comment on the Editorial “Embracing the Modern Biochemistry of Brain Metabolism” (2025)
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A Bird's‐Eye View of Glycolytic Upregulation in Activated Brain: The Major Fate of Lactate Is Release From Activated Tissue, Not Shuttling to Nearby Neurons (2025)
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A budget for brain metabolic water production by glucose catabolism during rest, rises in activity and sleep (2025)
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Reduced removal of waste products from energy metabolism takes center stage in human brain aging (2025)
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Setting standards for brain collection procedures in metabolomic studies (2025)
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Does hyperphenylalaninemia induce brain glucose hypometabolism? Cerebral spinal fluid findings in treated adult phenylketonuric patients (2024)
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Does Hyperphenylalaninemia Induce Brain Glucose Hypometabolism? Cerebral Spinal Fluid (CSF) Findings in Treated Adult Phenylketonuric (PKU) Patients (2024)
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Brain energy metabolism: A roadmap for future research (2024)
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A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments (2023)
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Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, <i>p</i>CO<sub>2</sub>, and <i>p</i>O<sub>2</sub> (2023)
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A tribute to Leif Hertz: The historical context of his pioneering studies of the roles of astrocytes in brain energy metabolism, neurotransmission, cognitive functions, and pharmacology identifies important, unresolved topics for future studies (2023)
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In vivo calibration of genetically encoded metabolite biosensors must account for metabolite metabolism during calibration and cellular volume (2023)
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Potential new roles for glycogen in epilepsy (2022)
Grants & Funding
- Endoplasmic reticulum stress in diabetic brain NIH Principal Investigator
- Neuroscience Research Center Core Facility at UAMS NIH Co-Investigator
- Functional Metabolism in Working Brain NIH Principal Investigator
- Astrocyte metabolite trafficking and brain imaging in Alzheimer model mice Alzheimer's Association Principal Investigator
- Glial Biology Gordon Research Conference NIH Co-Principal Investigator
- Functional activity in glia NIH Principal Investigator
- Astrocyte metabolite trafficking and brain imaging in Alzheimer model mice Alzheimer's Association Principal Investigator
- FUNCTIONAL METABOLIC ACTIVITY IN GLIA IN VIVO NIH Principal Investigator
Collaboration Network
Top Collaborators
Douglas L. Rothman
Yale University (US)
11 shared publications
- Brain energy metabolism: A roadmap for future research
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, <i>p</i>CO<sub>2</sub>, and <i>p</i>O<sub>2</sub>
- Mechanistic stoichiometric relationship between the rates of neurotransmission and neuronal glucose oxidation: Reevaluation of and alternatives to the pseudo‐malate‐aspartate shuttle model
- A tribute to Leif Hertz: The historical context of his pioneering studies of the roles of astrocytes in brain energy metabolism, neurotransmission, cognitive functions, and pharmacology identifies important, unresolved topics for future studies
- A Bird's‐Eye View of Glycolytic Upregulation in Activated Brain: The Major Fate of Lactate Is Release From Activated Tissue, Not Shuttling to Nearby Neurons
Showing 5 of 11 shared publications
Silvia Mangia
University of Minnesota (US)
5 shared publications
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, <i>p</i>CO<sub>2</sub>, and <i>p</i>O<sub>2</sub>
- A Bird's‐Eye View of Glycolytic Upregulation in Activated Brain: The Major Fate of Lactate Is Release From Activated Tissue, Not Shuttling to Nearby Neurons
- Comment on the Editorial “Embracing the Modern Biochemistry of Brain Metabolism”
- Reduced removal of waste products from energy metabolism takes center stage in human brain aging
- Brain maps of pCO2, pO2 and pH in aging via homeostatic modeling of neuroimaging data across the lifespan
Karin Borges
4 shared publications
- Brain energy metabolism: A roadmap for future research
- Potential new roles for glycogen in epilepsy
- Brain glycogen content is increased in the acute and interictal chronic stages of the mouse pilocarpine model of epilepsy
- Author response for "Brain energy metabolism: A roadmap for future research"
Kevin L. Behar
Yale University (US)
4 shared publications
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, <i>p</i>CO<sub>2</sub>, and <i>p</i>O<sub>2</sub>
- Mechanistic stoichiometric relationship between the rates of neurotransmission and neuronal glucose oxidation: Reevaluation of and alternatives to the pseudo‐malate‐aspartate shuttle model
- Reduced removal of waste products from energy metabolism takes center stage in human brain aging
- Brain maps of pCO2, pO2 and pH in aging via homeostatic modeling of neuroimaging data across the lifespan
Mary C. McKenna
3 shared publications
- Brain energy metabolism: A roadmap for future research
- A tribute to Leif Hertz: The historical context of his pioneering studies of the roles of astrocytes in brain energy metabolism, neurotransmission, cognitive functions, and pharmacology identifies important, unresolved topics for future studies
- Author response for "Brain energy metabolism: A roadmap for future research"
Mauro DiNuzzo
3 shared publications
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, <i>p</i>CO<sub>2</sub>, and <i>p</i>O<sub>2</sub>
- Reduced removal of waste products from energy metabolism takes center stage in human brain aging
- Brain maps of pCO2, pO2 and pH in aging via homeostatic modeling of neuroimaging data across the lifespan
Helene Benveniste
Yale University (US)
3 shared publications
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, <i>p</i>CO<sub>2</sub>, and <i>p</i>O<sub>2</sub>
- Reduced removal of waste products from energy metabolism takes center stage in human brain aging
- Brain maps of pCO2, pO2 and pH in aging via homeostatic modeling of neuroimaging data across the lifespan
Federico Giove
Enrico Fermi Center for Study and Research (IT)
3 shared publications
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, <i>p</i>CO<sub>2</sub>, and <i>p</i>O<sub>2</sub>
- Reduced removal of waste products from energy metabolism takes center stage in human brain aging
- Brain maps of pCO2, pO2 and pH in aging via homeostatic modeling of neuroimaging data across the lifespan
Shalom Michaeli
University of Minnesota (US)
3 shared publications
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, <i>p</i>CO<sub>2</sub>, and <i>p</i>O<sub>2</sub>
- Reduced removal of waste products from energy metabolism takes center stage in human brain aging
- Brain maps of pCO2, pO2 and pH in aging via homeostatic modeling of neuroimaging data across the lifespan
Sean‐Patrick Riechers
Northwestern University (US)
2 shared publications
- Neurons undergo pathogenic metabolic reprogramming in models of familial ALS
- Neurons undergo pathogenic metabolic reprograming in models of familial ALS
Jelena Mojsilovic-Petrovic
Northwestern University (US)
2 shared publications
- Neurons undergo pathogenic metabolic reprogramming in models of familial ALS
- Neurons undergo pathogenic metabolic reprograming in models of familial ALS
Mehraveh Garjani
Northwestern University (US)
2 shared publications
- Neurons undergo pathogenic metabolic reprogramming in models of familial ALS
- Neurons undergo pathogenic metabolic reprograming in models of familial ALS
Valentina Medvedeva
Northwestern University (US)
2 shared publications
- Neurons undergo pathogenic metabolic reprogramming in models of familial ALS
- Neurons undergo pathogenic metabolic reprograming in models of familial ALS
Casey Dalton
Northwestern University (US)
2 shared publications
- Neurons undergo pathogenic metabolic reprogramming in models of familial ALS
- Neurons undergo pathogenic metabolic reprograming in models of familial ALS
Robert G. Kalb
Northwestern University (US)
2 shared publications
- Neurons undergo pathogenic metabolic reprogramming in models of familial ALS
- Neurons undergo pathogenic metabolic reprograming in models of familial ALS
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