Earlier onset of cognitive deficits and an upregulated neuroinflammatory response in the chronic phase after stroke in obese mice
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Stroke is a neurovascular disease that frequently results in decreased motor and cognitive functioning. Obesity is a major risk factor associated with ischemic stroke and is thought to worsen the functional deficits observed after stroke. Previous findings from our laboratory suggest that worse motor deficits in obese animals may be a result from an exacerbated neuroinflammatory response. Most animal studies demonstrate an association between obesity and worse cognitive functioning after stroke. However, the mechanisms are not well studied. This study examines the neuroinflammatory response, ischemic brain tissue damage, and cognitive functioning in diet-induced obese mouse models during the chronic phase after ischemic stroke, defined as weeks after stroke. Our study found an earlier onset of cognitive deficits in obese mice after stroke compared to normal weight mice. We found no differences in the degree of brain damage in obese animals and normal weight animals 11 weeks after stroke, but observed higher levels of microgliosis in obese animals compared to normal weight animals. Due to the limitations of our study, additional studies should be done to assess the severity of cognitive deficits in obese animals compared to normal weight animals in the chronic phase after stroke. Further studies also need to be done to confirm our findings regarding the microglial response and degree of ischemic brain damage during the chronic phase.