Event Title

Behavioral Characterization of B6.HttQ175/+ Huntington’s Disease Model Mice

Co-Author(s)

Wes Solem, Will Hovander, Fiona Kinsella, and Jeffrey Carroll

Research Mentor(s)

Jeffrey Carroll

Description

Huntington’s disease (HD) is a fatal autosomal dominant neurodegenerative disease caused by a polyglutamine-coding (CAGs) repeat expansion in the Huntingtin (HTT) gene. The length of polyglutamine repeats are inversely correlated with age of disease onset. HD is defined by a triad of symptoms including cognitive impairment, movement disorders, and mood changes. HD is characterized by the loss of predominantly medium-sized spiny neurons (MSNs) in the striatum which can lead to motor dysfunctions in HD patients. Cognitive and psychiatric changes can appear 10-15 years prior to the onset of motor symptoms of HD. An important advancement in our understanding of HD derives from knock-in HD mouse models that capture the characteristics of human HD. Our previous research has been focused on characterizing behavioral phenotypes in B6.HttQ111/+ mice which have 111 glutamine repeats and display anxiety and apathetic phenotypes beginning around 9 months of age. Here, we began early characterization of the progression of these same phenotypes in B6.HttQ175/+ HD mice, which harbor 175 glutamine repeats in the mutant allele. We used an open field task to measure exploratory behavior as a proxy for anxiety and a balance beam to measure subtle motor deficits in the same mice at 3- and 6-months of age. We will discuss the phenotypic progression and the implications for using the B6.HttQ175/+ mouse model for preclinical HD research.

Document Type

Event

Start Date

16-5-2018 12:00 AM

End Date

16-5-2018 12:00 AM

Location

BRAIN, Behavioral Neuroscience

Comments

Outstanding Poster Award Recipient

Rights

Copying of this document in whole or in part is allowable only for scholarly purposes. It is understood, however, that any copying or publication of this document for commercial purposes, or for financial gain, shall not be allowed without the author’s written permission.

Language

English

Format

application/pdf

This document is currently not available here.

Share

COinS
 
May 16th, 12:00 AM May 16th, 12:00 AM

Behavioral Characterization of B6.HttQ175/+ Huntington’s Disease Model Mice

BRAIN, Behavioral Neuroscience

Huntington’s disease (HD) is a fatal autosomal dominant neurodegenerative disease caused by a polyglutamine-coding (CAGs) repeat expansion in the Huntingtin (HTT) gene. The length of polyglutamine repeats are inversely correlated with age of disease onset. HD is defined by a triad of symptoms including cognitive impairment, movement disorders, and mood changes. HD is characterized by the loss of predominantly medium-sized spiny neurons (MSNs) in the striatum which can lead to motor dysfunctions in HD patients. Cognitive and psychiatric changes can appear 10-15 years prior to the onset of motor symptoms of HD. An important advancement in our understanding of HD derives from knock-in HD mouse models that capture the characteristics of human HD. Our previous research has been focused on characterizing behavioral phenotypes in B6.HttQ111/+ mice which have 111 glutamine repeats and display anxiety and apathetic phenotypes beginning around 9 months of age. Here, we began early characterization of the progression of these same phenotypes in B6.HttQ175/+ HD mice, which harbor 175 glutamine repeats in the mutant allele. We used an open field task to measure exploratory behavior as a proxy for anxiety and a balance beam to measure subtle motor deficits in the same mice at 3- and 6-months of age. We will discuss the phenotypic progression and the implications for using the B6.HttQ175/+ mouse model for preclinical HD research.