Enriched environment enhances β-adrenergic signaling to prevent microglia inflammation by amyloid-β

Research output: Contribution to journal › Journal article › Research › peer-review

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Enriched environment enhances β-adrenergic signaling to prevent microglia inflammation by amyloid-β. / Xu, Huixin; Rajsombath, Molly M; Weikop, Pia; Selkoe, Dennis J.

In: EMBO Molecular Medicine, Vol. 10, No. 9, e8931, 2018.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Xu, H, Rajsombath, MM, Weikop, P & Selkoe, DJ 2018, 'Enriched environment enhances β-adrenergic signaling to prevent microglia inflammation by amyloid-β', EMBO Molecular Medicine, vol. 10, no. 9, e8931. https://doi.org/10.15252/emmm.201808931

APA

Xu, H., Rajsombath, M. M., Weikop, P., & Selkoe, D. J. (2018). Enriched environment enhances β-adrenergic signaling to prevent microglia inflammation by amyloid-β. EMBO Molecular Medicine, 10(9), [e8931]. https://doi.org/10.15252/emmm.201808931

Vancouver

Xu H, Rajsombath MM, Weikop P, Selkoe DJ. Enriched environment enhances β-adrenergic signaling to prevent microglia inflammation by amyloid-β. EMBO Molecular Medicine. 2018;10(9). e8931. https://doi.org/10.15252/emmm.201808931

Author

Xu, Huixin ; Rajsombath, Molly M ; Weikop, Pia ; Selkoe, Dennis J. / Enriched environment enhances β-adrenergic signaling to prevent microglia inflammation by amyloid-β. In: EMBO Molecular Medicine. 2018 ; Vol. 10, No. 9.

Bibtex

@article{f9ccb835cea64c2aba8cb6db2a37e866,

title = "Enriched environment enhances β-adrenergic signaling to prevent microglia inflammation by amyloid-β",

abstract = "Environmental enrichment (EE) is a rodent behavioral paradigm that can model the cognitive benefits to humans associated with intellectual activity and exercise. We recently discovered EE's anti-inflammatory protection of brain microglia against soluble oligomers of human amyloid β-protein (oAβ). Mechanistically, we report that the key factor in microglial protection by EE is chronically enhanced β-adrenergic signaling. Quantifying microglial morphology and inflammatory RNA profiles revealed that mice in standard housing (SH) fed the β-adrenergic agonist isoproterenol experienced similar protection of microglia against oAβ-induced inflammation as did mice in EE Conversely, mice in EE fed the β-adrenergic antagonist propranolol lost microglial protection against oAβ. Mice lacking β1/β2-adrenergic receptors showed no protection of microglia by EE In SH mice, quantification of norepinephrine in hippocampus and interstitial fluid showed that oAβ disrupted norepinephrine homeostasis, and microglial-specific analysis of β2-adrenergic receptors indicated a decreased receptor level. Both features were rescued by EE Thus, enhanced β-adrenergic signaling at the ligand and receptor levels mediates potent benefits of EE on microglial inflammation induced by human Aβ oligomers in vivo.",

author = "Huixin Xu and Rajsombath, {Molly M} and Pia Weikop and Selkoe, {Dennis J}",

note = "{\textcopyright} 2018 The Authors. Published under the terms of the CC BY 4.0 license.",

year = "2018",

doi = "10.15252/emmm.201808931",

language = "English",

volume = "10",

journal = "EMBO Molecular Medicine",

issn = "1757-4676",

publisher = "Wiley-Blackwell",

number = "9",

}

RIS

TY - JOUR

T1 - Enriched environment enhances β-adrenergic signaling to prevent microglia inflammation by amyloid-β

AU - Xu, Huixin

AU - Rajsombath, Molly M

AU - Weikop, Pia

AU - Selkoe, Dennis J

PY - 2018

Y1 - 2018

N2 - Environmental enrichment (EE) is a rodent behavioral paradigm that can model the cognitive benefits to humans associated with intellectual activity and exercise. We recently discovered EE's anti-inflammatory protection of brain microglia against soluble oligomers of human amyloid β-protein (oAβ). Mechanistically, we report that the key factor in microglial protection by EE is chronically enhanced β-adrenergic signaling. Quantifying microglial morphology and inflammatory RNA profiles revealed that mice in standard housing (SH) fed the β-adrenergic agonist isoproterenol experienced similar protection of microglia against oAβ-induced inflammation as did mice in EE Conversely, mice in EE fed the β-adrenergic antagonist propranolol lost microglial protection against oAβ. Mice lacking β1/β2-adrenergic receptors showed no protection of microglia by EE In SH mice, quantification of norepinephrine in hippocampus and interstitial fluid showed that oAβ disrupted norepinephrine homeostasis, and microglial-specific analysis of β2-adrenergic receptors indicated a decreased receptor level. Both features were rescued by EE Thus, enhanced β-adrenergic signaling at the ligand and receptor levels mediates potent benefits of EE on microglial inflammation induced by human Aβ oligomers in vivo.

AB - Environmental enrichment (EE) is a rodent behavioral paradigm that can model the cognitive benefits to humans associated with intellectual activity and exercise. We recently discovered EE's anti-inflammatory protection of brain microglia against soluble oligomers of human amyloid β-protein (oAβ). Mechanistically, we report that the key factor in microglial protection by EE is chronically enhanced β-adrenergic signaling. Quantifying microglial morphology and inflammatory RNA profiles revealed that mice in standard housing (SH) fed the β-adrenergic agonist isoproterenol experienced similar protection of microglia against oAβ-induced inflammation as did mice in EE Conversely, mice in EE fed the β-adrenergic antagonist propranolol lost microglial protection against oAβ. Mice lacking β1/β2-adrenergic receptors showed no protection of microglia by EE In SH mice, quantification of norepinephrine in hippocampus and interstitial fluid showed that oAβ disrupted norepinephrine homeostasis, and microglial-specific analysis of β2-adrenergic receptors indicated a decreased receptor level. Both features were rescued by EE Thus, enhanced β-adrenergic signaling at the ligand and receptor levels mediates potent benefits of EE on microglial inflammation induced by human Aβ oligomers in vivo.

U2 - 10.15252/emmm.201808931

DO - 10.15252/emmm.201808931

M3 - Journal article

C2 - 30093491

VL - 10

JO - EMBO Molecular Medicine

JF - EMBO Molecular Medicine

SN - 1757-4676

IS - 9

M1 - e8931

ER -

ID: 203406690

Center for Translational Neuromedicine