The effects of caffeine on ischemic neuronal injury as determined by magnetic resonance imaging and histopathology
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2016, NeuropharmacologyCitation Excerpt :Interestingly, chronic administration of adenosine receptor antagonists induced a reverse effect. Both caffeine and DPCPX given chronically weeks before an ischemic insult reduced the neuronal injury assessed by magnetic resonance imaging and histopathological examination in rats and gerbils (Rudolphi et al., 1989; Sutherland et al., 1991; von Lubitz et al., 1994a). It has been suggested that the beneficial effects seen after chronic administration of adenosine antagonists may be due to up-regulation of A1 receptors (Jacobson et al., 1996).
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2014, International Review of NeurobiologyCaffeine prevents cognitive impairment induced by chronic psychosocial stress and/or high fat-high carbohydrate diet
2013, Behavioural Brain ResearchCitation Excerpt :Thus, it seems that the low chronic dose of caffeine is acting as a protector rather than promoter of memory function. The ability of caffeine to prevent the effect of stress and/or WD is in agreement with previously reported beneficial effect of caffeine on memory impairment associated with ischemic neuronal injury [67], Alzheimer's disease [31], Parkinson's disease [30], attention deficit hyperactivity disorder [68], age-related cognitive decline [61], scopolamine-induced amnesia [69], and sleep deprivation [34,35]. Memory impairment and associated molecular changes in stress or WD are similar to changes seen in many of these conditions.
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2013, Tea in Health and Disease PreventionAbnormalities in the brain of streptozotocin-induced type 1 diabetic rats revealed by diffusion tensor imaging
2012, NeuroImage: ClinicalCitation Excerpt :It has been suggested that diabetic brain damage are secondary to vascular complications, such as increased permeability of microvasculature, high plasma osmolality and hypoperfusion (Jakus and Rietbrock, 2004). Interestingly, the striatum and frontal cortex, the two regions most affected by STZ-treatment, are also the regions known to be especially susceptible to ischemic damage (Lei et al., 1998; Sutherland et al., 1991). In addition, the pathohistological changes in the striatum and cortex we observed in the STZ-induced rats showed resemblance to what had been reported for rats subjected to chronic cerebral hypoperfusion (Chen et al., 2011; Shibata et al., 2004).