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- W1982842978 abstract "A history of stroke (cerebral ischemia) can increase an individual's risk of Alzheimer's Disease and is associated with an earlier age at onset of dementia. Furthermore, evidence of stroke pathology is present in one third of cases at post mortem (Kalaria et al, 2000). This study sought to determine whether stroke alters the expression and processing of amyloid precursor protein (APP) and amyloid production. Three month old male mutant APP mice (J9a) underwent an ischemic stroke induced by transient middle cerebral artery occlusion with an intraluminal thread. After 24 hour (n = 16) or 1 month survival (n = 19) brains, one cohort was processed for immunohistochemistry and another cohort underwent biochemical analysis using Western or dot blots. The levels of full length APP, C-terminal APP fragments and oligomeric amyloid were measured in the contralateral (control) and ipsilateral (ischemic) hemispheres and compared. Alterations in the cellular localisation and levels of APP and amyloid-β in the ischemic and contralateral striatum were determined. Levels of full-length APP and oligomeric amyloid were significantly increased 24 hours following ischaemia compared with the contralateral striatum (APP, p = 0.003; amyloid p = 0.045), whereas levels of APP c-terminal fragments were unaltered. In contrast, at 1month in response to stroke there was a significant increase in the level of C99 (p = 0.0356) whereas there was a significant reduction in the level of oligomeric amyloid (p = 0.004) and no change in the levels of full-length APP. At 24 hours in response to stroke, there was a marked increase in neuronal APP, whereas there were no gross changes in amyloid-β immunostaining. One month following stroke, there was an accumulation of APP in areas of ischaemic damage in the striatum that paralleled an accumulation of amyloid-β immunostaining within cells and the extracellular space. The results indicate that amyloidogenic processing of APP and amyloid up-regulation occurs in response to stroke. This suggests that stroke is associated with increased production of β-amyloid by influencing APP metabolism, which may link the role of ischemic insults to the pathogenesis of AD." @default.
- W1982842978 created "2016-06-24" @default.
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- W1982842978 date "2010-07-01" @default.
- W1982842978 modified "2023-09-27" @default.
- W1982842978 title "P2-343: Stroke increases oligomeric amyloid and amyloid deposition in mutant APP (J9a) mice" @default.
- W1982842978 doi "https://doi.org/10.1016/j.jalz.2010.05.1394" @default.
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