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Ellagic acid rescues motor and cognitive deficits in the R6/2 mouse model of Huntington's disease by lowering mutant huntingtin protein

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Abstract

Huntington's disease (HD) is a genetic neurodegenerative disorder caused by a highly polymorphic CAG trinucleotide repeat expansion encoding an extended polyglutamine (polyQ) tract at the N-terminus of huntingtin protein (HTT). The polyQ tract promotes the formation of toxic oligomers and aggregates of HTT, which leads to neuronal dysfunction and death. Therapies to lower mutant HTT (mHTT) and its aggregates appear to be the most promising strategies. Ellagic acid (EA) has been marketed as a dietary supplement with various claimed benefits and neuroprotective effects on several neurodegenerative disorders, while its effect on mHTT pathology is still unknown. Here we reported that EA significantly attenuated motor and cognitive deficits in R6/2 mice. Moreover, EA significantly lowered mHTT levels, reduced neuroinflammation, rescued synapse loss, and decreased oxidative stress in R6/2 mouse brains. These findings indicated that EA has promising therapeutic potential for HD treatment.

Graphical abstract: Ellagic acid rescues motor and cognitive deficits in the R6/2 mouse model of Huntington's disease by lowering mutant huntingtin protein

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Article information


Submitted
12 Sep 2019
Accepted
16 Jan 2020
First published
16 Jan 2020

Food Funct., 2020, Advance Article
Article type
Paper

Ellagic acid rescues motor and cognitive deficits in the R6/2 mouse model of Huntington's disease by lowering mutant huntingtin protein

X. Sun, J. Zhu, X. Sun, M. Ji, X. Yu and R. Liu, Food Funct., 2020, Advance Article , DOI: 10.1039/C9FO02131K

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