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Heliyon. 2018 Jan 18;4(1):e00508. doi: 10.1016/j.heliyon.2018.e00508. eCollection 2018 Jan.

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

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Department of Biology and Chemistry, Liberty University, Lynchburg, VA, 24515, USA.
Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, 21224, USA.
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
The Leslie and Susan Gonda Multidisciplinary Brain Research Center, Bar-Ilan University, Ramat-Gan, Israel.
The Paul Feder Laboratory on Alzheimer's Disease Research, Israel.


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.


Neurology; Neuroscience

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