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Low on energy? An energy supply-demand perspective on stress and depression

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Low on energy? An energy supply-demand perspective on stress and depression. / Østergaard, Leif; Jørgensen, Martin Balslev; Knudsen, Gitte Moos.

In: Neuroscience and Biobehavioral Reviews, Vol. 94, 01.11.2018, p. 248-270.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperReviewResearchpeer-review

Harvard

Østergaard, L, Jørgensen, MB & Knudsen, GM 2018, 'Low on energy? An energy supply-demand perspective on stress and depression', Neuroscience and Biobehavioral Reviews, vol. 94, pp. 248-270. https://doi.org/10.1016/j.neubiorev.2018.08.007

APA

Østergaard, L., Jørgensen, M. B., & Knudsen, G. M. (2018). Low on energy? An energy supply-demand perspective on stress and depression. Neuroscience and Biobehavioral Reviews, 94, 248-270. https://doi.org/10.1016/j.neubiorev.2018.08.007

CBE

MLA

Østergaard, Leif, Martin Balslev Jørgensen and Gitte Moos Knudsen. "Low on energy? An energy supply-demand perspective on stress and depression". Neuroscience and Biobehavioral Reviews. 2018, 94. 248-270. https://doi.org/10.1016/j.neubiorev.2018.08.007

Vancouver

Østergaard L, Jørgensen MB, Knudsen GM. Low on energy? An energy supply-demand perspective on stress and depression. Neuroscience and Biobehavioral Reviews. 2018 Nov 1;94:248-270. https://doi.org/10.1016/j.neubiorev.2018.08.007

Author

Østergaard, Leif ; Jørgensen, Martin Balslev ; Knudsen, Gitte Moos. / Low on energy? An energy supply-demand perspective on stress and depression. In: Neuroscience and Biobehavioral Reviews. 2018 ; Vol. 94. pp. 248-270.

Bibtex

@article{6a01d154726048e790955fb57c31428d,
title = "Low on energy? An energy supply-demand perspective on stress and depression",
abstract = "Are energy demands too high, or our energy resources either too low or inappropriately prioritized, as we develop stress and/or depression? We review evidence of dysregulated cellular energy homeostasis and energy depletion in stress and depression, identifying factors that might limit energy substrate availability. Resetting of cellular energy-sensors, splanchnic hypoxia, and catecholamine effects on blood viscosity emerge as mechanisms that might disrupt normal energy homeostasis, accelerate cell injury, and cause depression-like symptoms in severe or prolonged stress. In particular, a vicious cycle of capillary dysfunction, cellular hypoxia, and inflammation emerges as a mechanism, by which prolonged stress might accelerate the development of diseases, including depression, in later life. Oxygen is a substrate for both serotonin- and ATP-synthesis, and the review therefore analyzes evidence of reduced oxygen availability in neurological diseases with high incidence of depression. Blood supply and oxygen availability are also keys to the inference of neuronal activity by functional neuroimaging. We review how neurotransmitters interfere with blood flow regulation, affecting interpretations of neuroimaging studies in stress and depression.",
keywords = "Alzheimer's Disease (AD), Blood viscosity, Capillary dysfunction, Cardiovascular disease, Catecholamines, Cerebral small vessel disease (SVD), Co-morbidity, Cortisol, Early life stress, Functional magnetic resonance imaging (fMRI), Glutamate, Glycocalyx, Gut, Hemorheology, Hippocampus, Hypoxia, Inflammation, Major depressive disorder(MDD), Neurodegeneration, Neuroimaging, Pathophysiology, Pericyte, Serotonin, Stress, Trophic support, White matter hyperintensities (WMHs)",
author = "Leif {\O}stergaard and J{\o}rgensen, {Martin Balslev} and Knudsen, {Gitte Moos}",
year = "2018",
month = nov,
day = "1",
doi = "10.1016/j.neubiorev.2018.08.007",
language = "English",
volume = "94",
pages = "248--270",
journal = "Neuroscience & Biobehavioral Reviews",
issn = "0149-7634",
publisher = "Pergamon Press",

}

RIS

TY - JOUR

T1 - Low on energy? An energy supply-demand perspective on stress and depression

AU - Østergaard, Leif

AU - Jørgensen, Martin Balslev

AU - Knudsen, Gitte Moos

PY - 2018/11/1

Y1 - 2018/11/1

N2 - Are energy demands too high, or our energy resources either too low or inappropriately prioritized, as we develop stress and/or depression? We review evidence of dysregulated cellular energy homeostasis and energy depletion in stress and depression, identifying factors that might limit energy substrate availability. Resetting of cellular energy-sensors, splanchnic hypoxia, and catecholamine effects on blood viscosity emerge as mechanisms that might disrupt normal energy homeostasis, accelerate cell injury, and cause depression-like symptoms in severe or prolonged stress. In particular, a vicious cycle of capillary dysfunction, cellular hypoxia, and inflammation emerges as a mechanism, by which prolonged stress might accelerate the development of diseases, including depression, in later life. Oxygen is a substrate for both serotonin- and ATP-synthesis, and the review therefore analyzes evidence of reduced oxygen availability in neurological diseases with high incidence of depression. Blood supply and oxygen availability are also keys to the inference of neuronal activity by functional neuroimaging. We review how neurotransmitters interfere with blood flow regulation, affecting interpretations of neuroimaging studies in stress and depression.

AB - Are energy demands too high, or our energy resources either too low or inappropriately prioritized, as we develop stress and/or depression? We review evidence of dysregulated cellular energy homeostasis and energy depletion in stress and depression, identifying factors that might limit energy substrate availability. Resetting of cellular energy-sensors, splanchnic hypoxia, and catecholamine effects on blood viscosity emerge as mechanisms that might disrupt normal energy homeostasis, accelerate cell injury, and cause depression-like symptoms in severe or prolonged stress. In particular, a vicious cycle of capillary dysfunction, cellular hypoxia, and inflammation emerges as a mechanism, by which prolonged stress might accelerate the development of diseases, including depression, in later life. Oxygen is a substrate for both serotonin- and ATP-synthesis, and the review therefore analyzes evidence of reduced oxygen availability in neurological diseases with high incidence of depression. Blood supply and oxygen availability are also keys to the inference of neuronal activity by functional neuroimaging. We review how neurotransmitters interfere with blood flow regulation, affecting interpretations of neuroimaging studies in stress and depression.

KW - Alzheimer's Disease (AD)

KW - Blood viscosity

KW - Capillary dysfunction

KW - Cardiovascular disease

KW - Catecholamines

KW - Cerebral small vessel disease (SVD)

KW - Co-morbidity

KW - Cortisol

KW - Early life stress

KW - Functional magnetic resonance imaging (fMRI)

KW - Glutamate

KW - Glycocalyx

KW - Gut

KW - Hemorheology

KW - Hippocampus

KW - Hypoxia

KW - Inflammation

KW - Major depressive disorder(MDD)

KW - Neurodegeneration

KW - Neuroimaging

KW - Pathophysiology

KW - Pericyte

KW - Serotonin

KW - Stress

KW - Trophic support

KW - White matter hyperintensities (WMHs)

UR - http://www.scopus.com/inward/record.url?scp=85053800716&partnerID=8YFLogxK

U2 - 10.1016/j.neubiorev.2018.08.007

DO - 10.1016/j.neubiorev.2018.08.007

M3 - Review

C2 - 30145282

AN - SCOPUS:85053800716

VL - 94

SP - 248

EP - 270

JO - Neuroscience & Biobehavioral Reviews

JF - Neuroscience & Biobehavioral Reviews

SN - 0149-7634

ER -