Gerald A. Dienel
UAMS Contingent Worker
Also affiliated: National Institutes of Health (1995–1996); Deaconess Hospital (1978); NewYork–Presbyterian Hospital (1984–1986); Harvard University (1977–1978); University of New Mexico (2016–2025); Cornell University (1980–1986); Columbia University Irving Medical Center (2005); University of Arkansas Medical Center (1999–2025); Burke Rehabilitation Hospital (1980–1986); University of Rochester Medicine (2005); United States Public Health Service (1987–1990); Deaconess Hospital (1977–1981); National Institute of Neurological Disorders and Stroke (1995); Burke Medical Research Institute (1980); Office of Extramural Research (1996); National Institute of Mental Health (1985–2015)
Faculty Researcher
Neurology, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Gerald A. Dienel's research focuses on brain energy metabolism, particularly the interplay between neuronal activity, glucose utilization, and pH homeostasis. His work investigates how nonoxidative glycolysis and glycogenolysis contribute to compensating for increased proton production during brain activation, thereby maintaining physiological balance. Dienel has explored the functional role of aerobic glycolysis in interpreting neuroimaging signals and has examined potential new roles for glycogen in epilepsy.
His research also addresses methodological concerns in neuroscience, such as preventing artifacts during brain harvest to ensure accurate metabolic measurements. Dienel has investigated the mechanistic relationship between neurotransmission and neuronal glucose oxidation, reevaluating existing models and proposing alternatives. Furthermore, his work has touched upon pathogenic metabolic reprogramming in neurons within models of familial amyotrophic lateral sclerosis (ALS).
Dienel holds a high-impact researcher designation, evidenced by his h-index of 48 and over 10,705 citations across 150 publications. He leads a research group at the University of Arkansas for Medical Sciences.
Metrics
- h-index: 48
- Publications: 150
- Citations: 10,799
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
As listed on this researcher's institutional profile.
- 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
- FUNCTIONAL METABOLIC ACTIVITY IN GLIA IN VIVO NIH Principal Investigator
- Functional Metabolism in Working Brain NIH/Nat. Inst. of Neurological Disorders & Stroke Principal Investigator
Collaboration Network
Top Collaborators
- 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 9 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 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
- 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
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments.
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments.
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments.
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments.
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments.
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments.
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments
- A functional account of stimulation-based aerobic glycolysis and its role in interpreting BOLD signal intensity increases in neuroimaging experiments.
- 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
- 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
- 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
- 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
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