Open Access. Powered by Scholars. Published by Universities.®
Articles 1 - 2 of 2
Full-Text Articles in Medicine and Health Sciences
Evaluating White Matter Changes And Executive Function In Rat Models Of Mediodorsal Thalamic Stroke And Neuroinflammation, Jessica Garabon
Evaluating White Matter Changes And Executive Function In Rat Models Of Mediodorsal Thalamic Stroke And Neuroinflammation, Jessica Garabon
Electronic Thesis and Dissertation Repository
Recent literature has supported a relationship between vascular disease and its role in the progression of cognitive impairment. Previous studies have demonstrated that white matter inflammation (WMI) in the brain is a common pathological outcome following stroke. Moreover, WMI has been shown to be the strongest predictor of cognitive decline following stroke. Finally, previous work in our lab has demonstrated, using a rodent model of striatal stroke, that WMI is correlated with post-stroke cognitive impairment. The current study aimed to further investigate the role of WMI in post-stroke cognitive impairment by utilizing a mediodorsal thalamic (MD) stroke model in the …
An Investigation Into The Combined Effects Of Β-Amyloid Toxicity And Cerebral Ischemia On The Pathological Expression Of Gangliosides., Jeffrey D. Hepburn
An Investigation Into The Combined Effects Of Β-Amyloid Toxicity And Cerebral Ischemia On The Pathological Expression Of Gangliosides., Jeffrey D. Hepburn
Electronic Thesis and Dissertation Repository
Identifying mechanisms underlying the synergistic pathological interaction between stroke and Alzheimer’s disease (AD) can effectively guide future therapeutic strategies for these highly co-morbid conditions. Aberrant ganglioside expression marked by the pathological accumulation of ganglioside GM3 is common to stroke and AD, yet it is unclear whether GM3 is synergistically enhanced in a comorbid model, or if GM3 is a viable therapeutic target. Adult male Wistar rats received a unilateral ischemic striatal infarct via endothelin-1 (ET-1) injection alone or in combination with bilateral intracerebroventricular injection of the β-Amyloid 25-35 peptide (Aβ) to induce generalized Aβ toxicity (Aβ/ET-1). Animals were sacrificed after …