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Il-37 Reduces Neuroinflammation and Rescues Cognitive Impairment in an Alzheimer's Disease Model

46 Pages Posted: 7 Jun 2021 Publication Status: Review Complete

See all articles by Niklas Lonnemann

Niklas Lonnemann

TU Braunschweig - Department of Cellular Neurobiology

Shirin Hosseini

TU Braunschweig - Department of Cellular Neurobiology

Melanie Ohm

TU Braunschweig - Department of Cellular Neurobiology

Karsten Hiller

TU Braunschweig - Braunschweig Integrated Centre of Systems Biology

Charles A. Dinarello

University of Colorado at Denver - Department of Medicine; University of Colorado, Aurora - Department of Medicine

Martin Korte

TU Braunschweig - Department of Cellular Neurobiology

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Abstract

The anti-inflammatory cytokine Interleukin-37 (IL-37) is not expressed in the mouse. We used a human IL-37 (hIL-37tg) expressing mouse, which has been subjected to various models of local and systemic inflammation as well immunological challenges. Those studies demonstrate an immune modulatory role of IL-37. We investigated the functions of IL-37 in the CNS and explored the effects of IL-37 on neuronal architecture and function, microglia phenotype, cytokine production and behavior after inflammatory challenge with LPS-injection intraperitoneally. Reduced spine density, activated microglia phenotype and impaired long-term potentiation (LTP) in wild-type mice after LPS challenge was observed, whereas in contrast hIL-37tg mice showed no impairment. Furthermore, we crossed the hIL-37tg mouse into an animal model for Alzheimer’s disease (APP/PS1). We show the ability of IL-37 to limit inflammation in the brain following acute inflammatory events as well as the prevention of cognitive loss in a mouse model of AD.

Keywords: Alzheimer’s disease, Cognitive function, Interleukin-37, Neuroinflammation, Synaptic plasticity

Suggested Citation

Lonnemann, Niklas and Hosseini, Shirin and Ohm, Melanie and Hiller, Karsten and Dinarello, Charles A. and Korte, Martin, Il-37 Reduces Neuroinflammation and Rescues Cognitive Impairment in an Alzheimer's Disease Model. Available at SSRN: https://ssrn.com/abstract=3862015 or http://dx.doi.org/10.2139/ssrn.3862015
This version of the paper has not been formally peer reviewed.

Niklas Lonnemann

TU Braunschweig - Department of Cellular Neurobiology ( email )

Braunschweig
Germany

Shirin Hosseini

TU Braunschweig - Department of Cellular Neurobiology ( email )

Braunschweig
Germany

Melanie Ohm

TU Braunschweig - Department of Cellular Neurobiology ( email )

Braunschweig
Germany

Karsten Hiller

TU Braunschweig - Braunschweig Integrated Centre of Systems Biology ( email )

Abt-Jerusalem-Str. 7
Braunschweig, D-38106
Germany

Charles A. Dinarello

University of Colorado at Denver - Department of Medicine ( email )

Box 173364
1250 14th Street
Denver, CO 80217
United States

University of Colorado, Aurora - Department of Medicine ( email )

Martin Korte (Contact Author)

TU Braunschweig - Department of Cellular Neurobiology ( email )

Braunschweig
Germany

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