Behavioral Characterization of B6.HttQ175/+ Huntington’s Disease Model Mice
Research Mentor(s)
Carroll, Jeffrey B. (Jeffrey Bryan), 1977-
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
Department
Psychology
Genre/Form
student projects, posters
Subjects – Topical (LCSH)
Huntington's disease; Genetic psychology; Neuropsychology
Type
Image
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
Behavioral Characterization of B6.HttQ175/+ Huntington’s Disease Model Mice
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.
Comments
BRAIN, Behavioral Neuroscience, Outstanding Poster Award Recipient