Caspase-2 Deficiency Protects Mice from Behavioral Changes in Huntington's Disease
Author Information
Author(s): Jeffrey B. Carroll, Amber L. Southwell, Rona K. Graham, Jason P. Lerch, Dagmar E. Ehrnhoefer, Li-Ping Cao, Wei-Ning Zhang, Yu Deng, Nagat Bissada, Mark R. Henkelman, Michael R. Hayden
Primary Institution: University of British Columbia
Hypothesis
Does the absence of caspase-2 affect the progression of Huntington's disease in mice?
Conclusion
Mice lacking caspase-2 show improved behavioral symptoms of Huntington's disease without changes in pathological features.
Supporting Evidence
- Mice lacking caspase-2 performed at nearly wild-type levels on motor tasks.
- Behavioral improvements were observed in cognitive flexibility tasks.
- Pathological features such as striatal volume loss remained unchanged in caspase-2 deficient mice.
Takeaway
Mice without a specific protein called caspase-2 can move and think better when they have Huntington's disease, but their brains still get damaged.
Methodology
The study used YAC128 mice bred with caspase-2 deficient mice to assess behavioral and cognitive functions through various tasks.
Potential Biases
Potential bias in behavioral assessments due to the experimenter's knowledge of the genotypes.
Limitations
The study does not address the long-term effects of caspase-2 deficiency on overall health or other potential side effects.
Participant Demographics
Mice used were of the FVB/NJ strain, specifically bred for the study.
Statistical Information
P-Value
p = 0.0064
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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