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Motor, emotional and cognitive deficits in adult BACHD mice: a model for Huntington's disease
Yah-se K Abada1, Rudy Schreiber, Bart Ellenbroek
1EVOTEC AG, Essener Bogen 7, 22419 Hamburg, Germany. yah-se.abada@evotec.com
Insights
Huntington's disease (HD) BACHD mice exhibit motor, emotional, and cognitive deficits. These findings confirm BACHD mice as a valid model for studying HD and testing new therapies.
Area of Science:
- Neuroscience
- Genetics
- Animal Models
Background:
- Huntington's disease (HD) is a progressive neurodegenerative disorder characterized by motor, emotional, and cognitive impairments.
- HD is caused by an expanded polyglutamine tract in the huntingtin gene.
- Previous mouse models primarily focused on motor deficits, limiting comprehensive phenotyping.
Purpose of the Study:
- To conduct a comprehensive phenotypical assessment of motor, gait, emotional, and cognitive deficits in adult BACHD mice.
- To evaluate the utility of BACHD mice as a model for Huntington's disease.
Main Methods:
- 46 male BACHD mice (9-10 months old) were used, including wild-type and transgenic (+/T) groups.
- Motor function was assessed using Rotarod and Catwalk gait analysis.
- Emotional behavior was evaluated via zero-maze and fear conditioning; cognitive function was tested in a cross-maze strategy shifting task.
Main Results:
- Transgenic BACHD mice replicated previously observed motor deficits on the Rotarod and showed novel gait abnormalities on the Catwalk.
- BACHD mice displayed increased anxiety-like behavior (zero-maze) and heightened fear responses (fear conditioning).
- Impaired reversal learning and strategy shifting in the cross-maze indicated prefrontal-striatal pathway dysfunction.
Conclusions:
- BACHD mice exhibit a broad range of deficits relevant to Huntington's disease, demonstrating high face validity.
- This model is valuable for investigating HD pathogenesis and for preclinical testing of therapeutic interventions.
Rationale:
Huntington's disease (HD) is characterized by progressive motor dysfunction, emotional disturbances and cognitive deficits. It is a genetic disease caused by an elongation of the polyglutamine repeats in the huntingtin gene. Whereas HD is a complex disorder, previous studies in mice models have largely been confined to assessing motor deficits.
Objectives:
The aim of the present studies is a comprehensive phenotypical assessment of not only motor and gait deficits, but also of emotional and cognitive deficits in adult BACHD mice.
Material And Methods:
46 male BACHD mice between 9 and 10 months of age were used. Wild type (+/+) and transgenic (+/T) mice were tested for motor deficits on a Rotarod and Catwalk system. Emotional deficits were assessed with the zero-maze and fear conditioning tests. Cognitive deficits in a strategy shifting task were evaluated in a cross-maze test.
Results:
Comparing +/T and +/+ mice, we replicated the motor deficits in the transgenic mice that were previously described in the Rotarod test. For the first time, motor coordination imbalances in +/T animals are described in the Catwalk gait analysis system. +/T mice showed more anxiety-like behavior in the zero-maze test and a higher freezing response in the fear conditioning test. Reversal and strategy shifting impairments were demonstrated in the cross-maze, indicative of a disturbed prefrontal-striatal pathway.
Conclusion:
The results suggest that BACHD mice represent an animal model with a high degree of face validity for HD and may be very useful for testing novel therapeutic strategies.
