Gene-environment interactions modulating dementia and depression in a tandem repeat disorder
Cognitive deficits in HD, which culminate in dementia, create a major burden of disease. Furthermore, depression is the most common psychiatric symptom of HD and is estimated to develop in around half of all patients. Some changes to the brain of HD patients during the early stages of the disease are similar to changes that have been described in clinical dementia and depression.
Aim
- Investigate the molecular and cellular pathogenesis of dementia and depression in Huntington’s disease.
Using a transgenic mouse model of Huntington’s disease (HD), our group has made progress in understanding molecular and cellular mediators that lead to behavioural abnormalities, as well as environmental and pharmacological modulators.
We were the first group to demonstrate depression-like behaviors in an animal model of HD, and the first to relate cognitive dysfunction to in vivo deficits of experience-dependent neocortical plasticity. We were also the first to show that environmental factors, including environmental enrichment, exercise and stress, can modify onset and progression of HD.
Further studies are required to better understand the molecular and cellular pathogenesis of dementia and depression in HD.
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