Stroke-Related Translational Research

Caplan, Louis R.; Arenillas, Juan F.; Cramer, Steven C.; Joutel, Anne; Lo, Eng H.; Meschia, James F.; Savitz, Sean I; Tournier‐Lasserve, Elisabeth

doi:10.1001/archneurol.2011.99

Cited by 16 publications

(16 citation statements)

References 157 publications

(80 reference statements)

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“…Alternatively, we cannot exclude that higher doses could be needed for Polyman2 to reach the areas where MBL is deposited on the ischemic endothelium following pMCAo. However, since in the clinical setting areas lacking reperfusion are mingled with reperfused areas 1,15 , this limitation would not in principle prevent a possible efficacy in human stroke.…”

Section: Discussionmentioning

confidence: 99%

“…Here we document the pivotal role of MBL in cerebral ischemic injury by using different experimental models of focal ischemia. Since the degree of reperfusion is variable in the clinical setting 1,15 , we used both transient and permanent middle cerebral artery occlusion (tMCAo and pMCAo, respectively) in mice 9,10,12 . Additionally, an inhibitory monoclonal antibody against rat MBL-A 12,16 was also used in a reversible 3-vessel occlusion model (3-vo) in rats 17 .…”

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confidence: 99%

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Targeting Mannose-Binding Lectin Confers Long-Lasting Protection With a Surprisingly Wide Therapeutic Window in Cerebral Ischemia

et al. 2012

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Background The involvement of complement system in brain injury has been scarcely investigated. Here we document the pivotal role of mannose binding lectin (MBL), one of the recognition molecules of the lectin complement pathway, in brain ischemic injury. Methods and Results Focal cerebral ischemia was induced in mice (by permanent or transient middle cerebral artery occlusion) and rats (by 3-vessels occlusion). We first observed that MBL is deposited on ischemic vessels up to 48h after injury and that functional MBL/MASP2 complexes are increased. Next we demonstrated that: 1) MBL−/− mice are protected from both transient and permanent ischemic injury; 2) Polyman2, the newly synthesized mannosylated molecule selected for its binding to MBL, improves neurological deficits and infarct volume when given up to 24h after ischemia in mice; 3) anti-MBL-A antibody improves neurological deficits and infarct volume when given up to 18h after ischemia, as assessed following 28d in rats. Conclusions Our data show an important role for MBL in the pathogenesis of brain ischemic injury and provide a strong support to the concept that MBL inhibition may be a relevant therapeutic target in humans, one with a wide therapeutic window of application.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Targeting Mannose-Binding Lectin Confers Long-Lasting Protection With a Surprisingly Wide Therapeutic Window in Cerebral Ischemia

et al. 2012

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“…14 [10,11,12,13,14,15,16,17,18] in previous studies; this renders more difficult the demonstration of a favorable effect; the main end-point required global improvement of both neurological and functional measurements. In fact, in the ICTUS trial the mRs 0–2 was 29% vs .…”

Section: The Ictus Trialmentioning

confidence: 99%

The Role of Citicoline in Neuroprotection and Neurorepair in Ischemic Stroke

Álvarez-Sabín

Román

2013

Brain Sciences

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Advances in acute stroke therapy resulting from thrombolytic treatment, endovascular procedures, and stroke units have improved significantly stroke survival and prognosis; however, for the large majority of patients lacking access to advanced therapies stroke mortality and residual morbidity remain high and many patients become incapacitated by motor and cognitive deficits, with loss of independence in activities of daily living. Therefore, over the past several years, research has been directed to limit the brain lesions produced by acute ischemia (neuroprotection) and to increase the recovery, plasticity and neuroregenerative processes that complement rehabilitation and enhance the possibility of recovery and return to normal functions (neurorepair). Citicoline has therapeutic effects at several stages of the ischemic cascade in acute ischemic stroke and has demonstrated efficiency in a multiplicity of animal models of acute stroke. Long-term treatment with citicoline is safe and effective, improving post-stroke cognitive decline and enhancing patients’ functional recovery. Prolonged citicoline administration at optimal doses has been demonstrated to be remarkably well tolerated and to enhance endogenous mechanisms of neurogenesis and neurorepair contributing to physical therapy and rehabilitation.

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“…These findings suggest that a genetic predisposition combined with environmental stress (i.e., trauma, oral anticoagulant use, hypertension) may increase the risk of ICH [29]. This information may be important in determining ICH etiology in those patients without traditional ICH risk factors and it could have important preventive implications [33].…”

Section: Col4a1mentioning

confidence: 91%

Treatment Targets in Intracerebral Hemorrhage

Sangha

Gonzales

2011

Neurotherapeutics

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Intracerebral hemorrhage (ICH) imparts a higher mortality and morbidity than ischemic stroke. The therapeutic interventions that are currently available focus mainly on supportive care and secondary prevention. There is a paucity of evidence to support any one acute intervention that improves functional outcome. This chapter highlights current treatment targets for ICH based on the pathophysiology of the disease.

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Stroke-Related Translational Research

Cited by 16 publications

References 157 publications

Targeting Mannose-Binding Lectin Confers Long-Lasting Protection With a Surprisingly Wide Therapeutic Window in Cerebral Ischemia

Targeting Mannose-Binding Lectin Confers Long-Lasting Protection With a Surprisingly Wide Therapeutic Window in Cerebral Ischemia

The Role of Citicoline in Neuroprotection and Neurorepair in Ischemic Stroke

Treatment Targets in Intracerebral Hemorrhage

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