Metabolic plasticity of astrocytes and aging of the brain

Mitsuhiro Morita, Hiroko Ikeshima-Kataoka, Marko Kreft, Nina Vardjan, Robert Zorec, Mami Noda

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

As part of the blood-brain-barrier, astrocytes are ideally positioned between cerebral vasculature and neuronal synapses to mediate nutrient uptake from the systemic circulation. In addition, astrocytes have a robust enzymatic capacity of glycolysis, glycogenesis and lipid metabolism, managing nutrient support in the brain parenchyma for neuronal consumption. Here, we review the plasticity of astrocyte energy metabolism under physiologic and pathologic conditions, highlighting age-dependent brain dysfunctions. In astrocytes, glycolysis and glycogenesis are regulated by noradrenaline and insulin, respectively, while mitochondrial ATP production and fatty acid oxidation are influenced by the thyroid hormone. These regulations are essential for maintaining normal brain activities, and impairments of these processes may lead to neurodegeneration and cognitive decline. Metabolic plasticity is also associated with (re)activation of astrocytes, a process associated with pathologic events. It is likely that the recently described neurodegenerative and neuroprotective subpopulations of reactive astrocytes metabolize distinct energy substrates, and that this preference is supposed to explain some of their impacts on pathologic processes. Importantly, physiologic and pathologic properties of astrocytic metabolic plasticity bear translational potential in defining new potential diagnostic biomarkers and novel therapeutic targets to mitigate neurodegeneration and age-related brain dysfunctions.

Original languageEnglish
Article number941
JournalInternational journal of molecular sciences
Volume20
Issue number4
DOIs
Publication statusPublished - Feb 2 2019

Fingerprint

plastic properties
Astrocytes
brain
Plasticity
Brain
metabolism
Aging of materials
glycolysis
nutrients
lipid metabolism
Glycolysis
blood-brain barrier
synapses
insulin
Nutrients
hormones
adenosine triphosphate
biomarkers
impairment
fatty acids

All Science Journal Classification (ASJC) codes

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

Metabolic plasticity of astrocytes and aging of the brain. / Morita, Mitsuhiro; Ikeshima-Kataoka, Hiroko; Kreft, Marko; Vardjan, Nina; Zorec, Robert; Noda, Mami.

In: International journal of molecular sciences, Vol. 20, No. 4, 941, 02.02.2019.

Research output: Contribution to journalReview article

Morita, Mitsuhiro ; Ikeshima-Kataoka, Hiroko ; Kreft, Marko ; Vardjan, Nina ; Zorec, Robert ; Noda, Mami. / Metabolic plasticity of astrocytes and aging of the brain. In: International journal of molecular sciences. 2019 ; Vol. 20, No. 4.
@article{4bc8b2a126a042e48c9f2bf2026de4a2,
title = "Metabolic plasticity of astrocytes and aging of the brain",
abstract = "As part of the blood-brain-barrier, astrocytes are ideally positioned between cerebral vasculature and neuronal synapses to mediate nutrient uptake from the systemic circulation. In addition, astrocytes have a robust enzymatic capacity of glycolysis, glycogenesis and lipid metabolism, managing nutrient support in the brain parenchyma for neuronal consumption. Here, we review the plasticity of astrocyte energy metabolism under physiologic and pathologic conditions, highlighting age-dependent brain dysfunctions. In astrocytes, glycolysis and glycogenesis are regulated by noradrenaline and insulin, respectively, while mitochondrial ATP production and fatty acid oxidation are influenced by the thyroid hormone. These regulations are essential for maintaining normal brain activities, and impairments of these processes may lead to neurodegeneration and cognitive decline. Metabolic plasticity is also associated with (re)activation of astrocytes, a process associated with pathologic events. It is likely that the recently described neurodegenerative and neuroprotective subpopulations of reactive astrocytes metabolize distinct energy substrates, and that this preference is supposed to explain some of their impacts on pathologic processes. Importantly, physiologic and pathologic properties of astrocytic metabolic plasticity bear translational potential in defining new potential diagnostic biomarkers and novel therapeutic targets to mitigate neurodegeneration and age-related brain dysfunctions.",
author = "Mitsuhiro Morita and Hiroko Ikeshima-Kataoka and Marko Kreft and Nina Vardjan and Robert Zorec and Mami Noda",
year = "2019",
month = "2",
day = "2",
doi = "10.3390/ijms20040941",
language = "English",
volume = "20",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "4",

}

TY - JOUR

T1 - Metabolic plasticity of astrocytes and aging of the brain

AU - Morita, Mitsuhiro

AU - Ikeshima-Kataoka, Hiroko

AU - Kreft, Marko

AU - Vardjan, Nina

AU - Zorec, Robert

AU - Noda, Mami

PY - 2019/2/2

Y1 - 2019/2/2

N2 - As part of the blood-brain-barrier, astrocytes are ideally positioned between cerebral vasculature and neuronal synapses to mediate nutrient uptake from the systemic circulation. In addition, astrocytes have a robust enzymatic capacity of glycolysis, glycogenesis and lipid metabolism, managing nutrient support in the brain parenchyma for neuronal consumption. Here, we review the plasticity of astrocyte energy metabolism under physiologic and pathologic conditions, highlighting age-dependent brain dysfunctions. In astrocytes, glycolysis and glycogenesis are regulated by noradrenaline and insulin, respectively, while mitochondrial ATP production and fatty acid oxidation are influenced by the thyroid hormone. These regulations are essential for maintaining normal brain activities, and impairments of these processes may lead to neurodegeneration and cognitive decline. Metabolic plasticity is also associated with (re)activation of astrocytes, a process associated with pathologic events. It is likely that the recently described neurodegenerative and neuroprotective subpopulations of reactive astrocytes metabolize distinct energy substrates, and that this preference is supposed to explain some of their impacts on pathologic processes. Importantly, physiologic and pathologic properties of astrocytic metabolic plasticity bear translational potential in defining new potential diagnostic biomarkers and novel therapeutic targets to mitigate neurodegeneration and age-related brain dysfunctions.

AB - As part of the blood-brain-barrier, astrocytes are ideally positioned between cerebral vasculature and neuronal synapses to mediate nutrient uptake from the systemic circulation. In addition, astrocytes have a robust enzymatic capacity of glycolysis, glycogenesis and lipid metabolism, managing nutrient support in the brain parenchyma for neuronal consumption. Here, we review the plasticity of astrocyte energy metabolism under physiologic and pathologic conditions, highlighting age-dependent brain dysfunctions. In astrocytes, glycolysis and glycogenesis are regulated by noradrenaline and insulin, respectively, while mitochondrial ATP production and fatty acid oxidation are influenced by the thyroid hormone. These regulations are essential for maintaining normal brain activities, and impairments of these processes may lead to neurodegeneration and cognitive decline. Metabolic plasticity is also associated with (re)activation of astrocytes, a process associated with pathologic events. It is likely that the recently described neurodegenerative and neuroprotective subpopulations of reactive astrocytes metabolize distinct energy substrates, and that this preference is supposed to explain some of their impacts on pathologic processes. Importantly, physiologic and pathologic properties of astrocytic metabolic plasticity bear translational potential in defining new potential diagnostic biomarkers and novel therapeutic targets to mitigate neurodegeneration and age-related brain dysfunctions.

UR - http://www.scopus.com/inward/record.url?scp=85062017997&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85062017997&partnerID=8YFLogxK

U2 - 10.3390/ijms20040941

DO - 10.3390/ijms20040941

M3 - Review article

C2 - 30795555

AN - SCOPUS:85062017997

VL - 20

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 4

M1 - 941

ER -