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Related Concept Videos

Human Genetics01:28

Human Genetics

Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...

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Related Experiment Video

Updated: Jun 28, 2026

Biomarkers in an Animal Model for Revealing Neural, Hematologic, and Behavioral Correlates of PTSD
08:29

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Brain gene expression correlates with changes in behavior in the R6/1 mouse model of Huntington's disease.

A Hodges1, G Hughes, S Brooks

  • 1Department of Psychological Medicine, Wales School of Medicine, Cardiff University, Cardiff, United Kingdom.

Genes, Brain, and Behavior
|August 19, 2007
PubMed
Summary

Huntington's disease (HD) mouse models show early gene expression deficits. These molecular changes correlate with specific behavioral impairments, suggesting diverse assessments are needed for therapeutic trials.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Huntington's disease (HD) is a fatal inherited neurodegenerative disorder.
  • Early molecular hallmarks of HD include significant transcriptional deficits.
  • Animal models are crucial for studying HD pathogenesis.

Purpose of the Study:

  • To investigate changes in brain gene expression in the R6/1 mouse model of HD.
  • To correlate gene expression alterations with behavioral deficits over disease progression.
  • To assess the utility of different behavioral tasks in HD mouse models.

Main Methods:

  • Analysis of brain gene expression in R6/1 mice from 18 to 27 weeks.
  • Gene ontology analysis to identify altered biological pathways.
  • Behavioral testing including rotarod, locomotor activity, and exploratory behavior assessment.

Main Results:

  • Gene expression changes in R6/1 mice mirrored those in R6/2 models.
  • Downregulated genes impacted intracellular and electrical signaling pathways.
  • Upregulated genes were associated with lipid biosynthesis and RNA processes.
  • Specific gene expression changes correlated uniquely with individual behavioral deficits, not all.

Conclusions:

  • Early transcriptional deficits are a key feature of HD progression in mouse models.
  • Distinct gene expression alterations are linked to specific behavioral impairments.
  • Comprehensive behavioral assessments are essential for evaluating therapeutic efficacy in HD mouse models.