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Corticostriatal network dysfunction in Huntington's disease: Deficits in neural processing, glutamate transport, and
1Program in Neuroscience, Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA.
CNS Neuroscience & Therapeutics
|February 22, 2018
Summary
Huntington's disease (HD) disrupts communication between brain cells early on. Targeting glutamate and ascorbate in transgenic mouse models shows promise for improving neurobehavioral processing in HD.
Area of Science:
- Neuroscience
- Genetics
- Neurodegenerative Diseases
Background:
- Huntington's disease (HD) is a fatal neurodegenerative disorder.
- It stems from a single gene mutation, leading to dysfunctional neuronal connectivity.
Purpose of the Study:
- To review evidence of impaired corticostriatal connectivity in Huntington's disease.
- To focus on electrophysiological data from transgenic mouse models.
Main Methods:
- Analysis of electrophysiological signals in behaving transgenic mouse models.
- Examination of neuronal firing patterns and local field potential oscillations.
- Computational strategies to analyze corticostriatal information flow.
Main Results:
- Dysfunctional corticostriatal processing is evident in HD models.
- Mutant gene interactions, not just the gene itself, drive disruptions.
- Dysregulation of glutamate and ascorbate impacts communication.
Conclusions:
- HD impairs neuronal communication before significant cell loss.
- Restoring glutamate and ascorbate balance is crucial for therapeutic strategies.
- Further research is needed to understand behavioral modulation of corticostriatal pathways.