2016
DOI: 10.1177/0271678x16654920
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Chronic stress exposure following photothrombotic stroke is associated with increased levels of Amyloid beta accumulation and altered oligomerisation at sites of thalamic secondary neurodegeneration in mice

Abstract: Exposure to severe stress following stroke is recognised to complicate the recovery process. We have identified that stress can exacerbate the severity of post-stroke secondary neurodegeneration in the thalamus. In this study, we investigated whether exposure to stress could influence the accumulation of the neurotoxic protein Amyloid-β. Using an experimental model of focal cortical ischemia in adult mice combined with exposure to chronic restraint stress, we examined changes within the contra- and ipsilateral… Show more

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Cited by 44 publications
(49 citation statements)
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“…Animal studies allow for better control of confounding factors and direct examination of brain tissue. In earlier rodent studies, post-stroke Aβ deposits were found to be common, while the only published non-human primate study using marmosets identified no Aβ pathology in the thalamus in a 45-day follow-up post-stroke (14,25,35,43,47,52,53,58,59). We have previously demonstrated consistent post-stroke Aβ deposits in the thalamus of rats at 7 and 14 days after permanent MCAO (52,53,58,59).…”
Section: Discussionmentioning
confidence: 56%
“…Animal studies allow for better control of confounding factors and direct examination of brain tissue. In earlier rodent studies, post-stroke Aβ deposits were found to be common, while the only published non-human primate study using marmosets identified no Aβ pathology in the thalamus in a 45-day follow-up post-stroke (14,25,35,43,47,52,53,58,59). We have previously demonstrated consistent post-stroke Aβ deposits in the thalamus of rats at 7 and 14 days after permanent MCAO (52,53,58,59).…”
Section: Discussionmentioning
confidence: 56%
“…2). While there is evidence that Ab plaques are present in the chronic phases after stroke, in our model 14 days after the infraction, there is no evidence of plaques within the brain (Ong et al, 2016; van Groen, Puurunen, Maki, Sivenius, & Jolkkonen, 2005). We FIG URE 8 Increased expression of CD68 in both the PI territories and ipsilateral thalamus after stroke.…”
mentioning
confidence: 57%
“…Previous studies of microglia morphology post‐stroke have shown microglia “activation,” characterized by deramified cells with a generally amoeboid appearance. This phenotype was observed both in the PI area and in sites of SND, most notably within the thalamus, and has been shown to persist for several months post‐stroke (Jones et al, ; Ong et al, ; Zhang et al, ).…”
Section: Resultsmentioning
confidence: 99%
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