Its increasing incidence has led stroke to be the second leading cause of death worldwide. Despite significant advances in recanalization strategies, patients are still at risk for ischemia/reperfusion injuries in this pathophysiology, in which neuroinflammation is significantly involved. Research has shown that in the acute phase, neuroinflammatory cascades lead to apoptosis, disruption of the blood–brain barrier, cerebral edema, and hemorrhagic transformation, while in later stages, these pathways support tissue repair and functional recovery. The present review discusses the various cell types and the mechanisms through which neuroinflammation contributes to parenchymal injury and tissue repair, as well as therapeutic attempts made in vitro, in animal experiments, and in clinical trials which target neuroinflammation, highlighting future therapeutic perspectives.

The significant gain in life expectancy led to an increase in the incidence and prevalence of dementia. Although vascular risk factors have long and repeatedly been shown to increase the risk of Alzheimer’s Disease (AD), translating these findings into effective preventive measures has failed. In addition, the finding that incident ischemic stroke approximately doubles the risk of a patient to develop AD has been recently reinforced. Current knowledge and pathogenetic hypotheses of AD are discussed. The implication of oxidative stress in the development of AD is reviewed, with special emphasis on its sudden burst in the setting of acute ischemic stroke and the possible link between this increase in oxidative stress and consequent cognitive impairment. Current knowledge and future directions in the prevention and treatment of AD are discussed outlining the hypothesis of a possible beneficial effect of antioxidant treatment in acute ischemic stroke in delaying the onset/progression of dementia.

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Background and Objectives: The efficacy of hydroxy methyl glutaryl-coenzyme A reductase inhibitors (statins) in reducing the incidence of cardiovascular events pushed the target LDL-cholesterol (LDL-C) levels lower and lower in successive guidelines despite signals regarding potential cognitive side effects. We evaluated the relationship between cognitive impairment and LDL-C levels in elderly ischemic stroke patients. Materials and Methods: 29 ischemic stroke patients aged 65 and above with LDL-C levels ≤70 mg/dL, classified according to the TOAST criteria, underwent detailed neuropsychological testing comprising the MMSE test, Montreal Cognitive Assessment (MoCA) and Addenbrooke’s Cognitive Evaluation (ACE-III) test. Their performances were compared to those of 29 age-matched ischemic stroke patients with LDL-Cl levels >71 mg/dL. Results: The MMSE test failed to detect significant cognitive differences between the two groups. The MoCA and ACE-III tests detected impairments in visuo-spatial/executive function, attention, and recall/memory in patients with low LDL-C. A stepwise linear regression model of the ACE-III total scores revealed that LDL-cholesterol levels could contribute to 13.8% of the detected cognitive dysfunction, second in importance only to age, which contributed to 38.8% of the detected impairment. Conclusions: Physicians should be cautious when prescribing statins to elderly people. Hydrophilic ones may be preferred in cognitively impaired patients.

Introduction. Romania ranks third worldwide for stroke mortality. Although high blood pressure (BP) is a major risk factor for stroke incidence and determinant of outcome, the management of BP in acute stroke remains undefined. The present study assesses patients recruited into the ‘Efficacy of Nitric Oxide in Stroke’ (ENOS) trial from Romania, one of 19 participating countries. Methods. ENOS is an international multicentre prospective randomised controlled trial that is assessing the safety and efficacy of: (i) lowering BP with transdermal glyceryl trinitrate, and (ii) whether pre-stroke antihypertensive therapy should be continued or stopped temporarily, in acute ischaemic stroke or primary intracerebral haemorrhage (PICH). Interventions are given for 7 days and the primary outcome, modified Rankin Scale (mRS), is measured at 90 days. Results. 135 patients were recruited from 3 Romanian sites between March 2009 and August 2011; 56% of these patients were also in the continue-stop arm of the trial. In comparison with the Rest of the World (RoW), Romanian patients were recruited earlier (29 vs. 22 hr), had a higher rate of previous high BP (63 vs. 76%), had less severe stroke at baseline (Scandinavian Stroke Scale, SSS 37 vs. 43/58), were less likely to have a PICH (17 vs. 10%), and had more cases of no visible stroke lesions on baseline CT (27 vs. 49%). Impairment (SSS) at day 7 did not differ. As compared to RoW, the length of stay in hospital was shorter in Romania (14 vs. 9 days); the adjusted death rate at follow-up at 90 days was doubled (odds ratio 1.97, 95% confidence intervals 1.07-3.63) although this was not reflected by a difference in the adjusted rate of death or dependency (mRS>2) at 90 days (OR 1.04, 95% CI 0.66-1.63). Conclusion. ENOS will continue recruiting patients until the summer of 2013. The presented data show that enrolment is feasible in Romania and the trial has been found to be easy to manage and recruit into.