Astrocyte energy and neurotransmitter metabolism in Alzheimer's disease: Integration of the glutamate/GABA-glutamine cycle

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Astrocyte energy and neurotransmitter metabolism in Alzheimer's disease : Integration of the glutamate/GABA-glutamine cycle. / Andersen, Jens V.; Schousboe, Arne; Verkhratsky, Alexei.

In: Progress in Neurobiology, Vol. 217, 102331, 2022.

Research output: Contribution to journalReviewResearchpeer-review

Harvard

Andersen, JV, Schousboe, A & Verkhratsky, A 2022, 'Astrocyte energy and neurotransmitter metabolism in Alzheimer's disease: Integration of the glutamate/GABA-glutamine cycle', Progress in Neurobiology, vol. 217, 102331. https://doi.org/10.1016/j.pneurobio.2022.102331

APA

Andersen, J. V., Schousboe, A., & Verkhratsky, A. (2022). Astrocyte energy and neurotransmitter metabolism in Alzheimer's disease: Integration of the glutamate/GABA-glutamine cycle. Progress in Neurobiology, 217, [102331]. https://doi.org/10.1016/j.pneurobio.2022.102331

Vancouver

Andersen JV, Schousboe A, Verkhratsky A. Astrocyte energy and neurotransmitter metabolism in Alzheimer's disease: Integration of the glutamate/GABA-glutamine cycle. Progress in Neurobiology. 2022;217. 102331. https://doi.org/10.1016/j.pneurobio.2022.102331

Author

Andersen, Jens V. ; Schousboe, Arne ; Verkhratsky, Alexei. / Astrocyte energy and neurotransmitter metabolism in Alzheimer's disease : Integration of the glutamate/GABA-glutamine cycle. In: Progress in Neurobiology. 2022 ; Vol. 217.

Bibtex

@article{5c72ae2e15234ea9bcb8550bdedffb21,
title = "Astrocyte energy and neurotransmitter metabolism in Alzheimer's disease: Integration of the glutamate/GABA-glutamine cycle",
abstract = "Astrocytes contribute to the complex cellular pathology of Alzheimer's disease (AD). Neurons and astrocytes function in close collaboration through neurotransmitter recycling, collectively known as the glutamate/GABA-glutamine cycle, which is essential to sustain neurotransmission. Neurotransmitter recycling is intimately linked to astrocyte energy metabolism. In the course of AD, astrocytes undergo extensive metabolic remodeling, which may profoundly affect the glutamate/GABA-glutamine cycle. The consequences of altered astrocyte function and metabolism in relation to neurotransmitter recycling are yet to be comprehended. Metabolic alterations of astrocytes in AD deprive neurons of metabolic support, thereby contributing to synaptic dysfunction and neurodegeneration. In addition, several astrocyte-specific components of the glutamate/GABA-glutamine cycle, including glutamine synthesis and synaptic neurotransmitter uptake, are perturbed in AD. Integration of the complex astrocyte biology within the context of AD is essential for understanding the fundamental mechanisms of the disease, while restoring astrocyte metabolism may serve as an approach to arrest or even revert clinical progression of AD.",
keywords = "Alternative substrates, Astrogliosis, Dementia, Excitotoxicity, Mitochondria, Neurodegeneration, Neurotransmitter recycling",
author = "Andersen, {Jens V.} and Arne Schousboe and Alexei Verkhratsky",
note = "Funding Information: JVA gratefully acknowledges The Scholarship of Peter & Emma Thomsen (Denmark). ",
year = "2022",
doi = "10.1016/j.pneurobio.2022.102331",
language = "English",
volume = "217",
journal = "Progress in Neurobiology",
issn = "0301-0082",
publisher = "Pergamon Press",

}

RIS

TY - JOUR

T1 - Astrocyte energy and neurotransmitter metabolism in Alzheimer's disease

T2 - Integration of the glutamate/GABA-glutamine cycle

AU - Andersen, Jens V.

AU - Schousboe, Arne

AU - Verkhratsky, Alexei

N1 - Funding Information: JVA gratefully acknowledges The Scholarship of Peter & Emma Thomsen (Denmark).

PY - 2022

Y1 - 2022

N2 - Astrocytes contribute to the complex cellular pathology of Alzheimer's disease (AD). Neurons and astrocytes function in close collaboration through neurotransmitter recycling, collectively known as the glutamate/GABA-glutamine cycle, which is essential to sustain neurotransmission. Neurotransmitter recycling is intimately linked to astrocyte energy metabolism. In the course of AD, astrocytes undergo extensive metabolic remodeling, which may profoundly affect the glutamate/GABA-glutamine cycle. The consequences of altered astrocyte function and metabolism in relation to neurotransmitter recycling are yet to be comprehended. Metabolic alterations of astrocytes in AD deprive neurons of metabolic support, thereby contributing to synaptic dysfunction and neurodegeneration. In addition, several astrocyte-specific components of the glutamate/GABA-glutamine cycle, including glutamine synthesis and synaptic neurotransmitter uptake, are perturbed in AD. Integration of the complex astrocyte biology within the context of AD is essential for understanding the fundamental mechanisms of the disease, while restoring astrocyte metabolism may serve as an approach to arrest or even revert clinical progression of AD.

AB - Astrocytes contribute to the complex cellular pathology of Alzheimer's disease (AD). Neurons and astrocytes function in close collaboration through neurotransmitter recycling, collectively known as the glutamate/GABA-glutamine cycle, which is essential to sustain neurotransmission. Neurotransmitter recycling is intimately linked to astrocyte energy metabolism. In the course of AD, astrocytes undergo extensive metabolic remodeling, which may profoundly affect the glutamate/GABA-glutamine cycle. The consequences of altered astrocyte function and metabolism in relation to neurotransmitter recycling are yet to be comprehended. Metabolic alterations of astrocytes in AD deprive neurons of metabolic support, thereby contributing to synaptic dysfunction and neurodegeneration. In addition, several astrocyte-specific components of the glutamate/GABA-glutamine cycle, including glutamine synthesis and synaptic neurotransmitter uptake, are perturbed in AD. Integration of the complex astrocyte biology within the context of AD is essential for understanding the fundamental mechanisms of the disease, while restoring astrocyte metabolism may serve as an approach to arrest or even revert clinical progression of AD.

KW - Alternative substrates

KW - Astrogliosis

KW - Dementia

KW - Excitotoxicity

KW - Mitochondria

KW - Neurodegeneration

KW - Neurotransmitter recycling

U2 - 10.1016/j.pneurobio.2022.102331

DO - 10.1016/j.pneurobio.2022.102331

M3 - Review

C2 - 35872221

AN - SCOPUS:85135684171

VL - 217

JO - Progress in Neurobiology

JF - Progress in Neurobiology

SN - 0301-0082

M1 - 102331

ER -

ID: 318206027