Deficiency of Toll-like receptors 2, 3 or 4 extends life expectancy in Huntington's disease mice

Kathleen Griffioen; Mark P. Mattson; Eitan Okun

doi:10.1016/j.heliyon.2018.e00508

Deficiency of Toll-like receptors 2, 3 or 4 extends life expectancy in Huntington's disease mice

Kathleen Griffioen, Mark P. Mattson, Eitan Okun

The Mina and Everard Goodman Faculty of Life Sciences

Research output: Contribution to journal › Article › peer-review

25 Scopus citations

Abstract

Huntington's disease (HD), an autosomal dominant neurodegenerative disorder characterized by progressive striatal and cortical atrophy, has been strongly linked with neuroinflammation. Toll-like receptors, a family of innate immune receptors, are a major pathway for neuroinflammation with pleiotropic effects on neuronal plasticity and neurodevelopment. We assessed whether deficiency for TLRs 2, 3 or 4 affects life expectancy in the N171-82Q mouse model of HD. Our data indicate that homozygous TLRs 2 and 3 as well as heterozygous TLR4 deficiency significantly extends the life expectancy of HD mice. Our data suggest that multiple TLR pathways may be involved in the neuroinflammatory and degenerative processes during HD.

Original language	English
Article number	e00508
Journal	Heliyon
Volume	4
Issue number	1
DOIs	https://doi.org/10.1016/j.heliyon.2018.e00508
State	Published - Jan 2018

Bibliographical note

Publisher Copyright:
© 2018 The Authors

Funding

This work was supported by the Intramural Research Program of the National Institute on Aging , and the Paul Feder Laboratory for Research on Neurodegenerative Disorders .

Funders	Funder number
National Institute on Aging

Keywords

Neurology
Neuroscience

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.heliyon.2018.e00508

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abstract = "Huntington's disease (HD), an autosomal dominant neurodegenerative disorder characterized by progressive striatal and cortical atrophy, has been strongly linked with neuroinflammation. Toll-like receptors, a family of innate immune receptors, are a major pathway for neuroinflammation with pleiotropic effects on neuronal plasticity and neurodevelopment. We assessed whether deficiency for TLRs 2, 3 or 4 affects life expectancy in the N171-82Q mouse model of HD. Our data indicate that homozygous TLRs 2 and 3 as well as heterozygous TLR4 deficiency significantly extends the life expectancy of HD mice. Our data suggest that multiple TLR pathways may be involved in the neuroinflammatory and degenerative processes during HD.",

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Deficiency of Toll-like receptors 2, 3 or 4 extends life expectancy in Huntington's disease mice

Abstract

Bibliographical note

Funding

Keywords

UN SDGs

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