Neuroprotection for ischaemic stroke: Current status and challenges

Boring title - neuroprotection. It gives no sense of urgency. However if you told your doctor that the neuronal cascade of death was occurring right now in your brain, then maybe your doctor might consider doing something about it.  And no mention of Dr. Michael Tymianskis' comment. on the 1000+ failed neuroprotection drugs. I'm not going to compare this to my 177 hyperacute therapies. Your doctor should know about all of them and have contacted researchers to test out those possibilities.
http://www.sciencedirect.com/science/article/pii/S016372581400165X

• Antonio Moretti,
• Federica Ferrari,
• Roberto F. Villa^,

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DOI: 10.1016/j.pharmthera.2014.09.003

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Abstract

Stroke is the third cause of death worldwide and the main cause of chronic, severe adult disability. We focus on acute ischaemic stroke, which accounts for approximately 80% of all strokes. The current therapy aims at restoring cerebral blood flow within a narrow time window in order to prevent damaging the “penumbra” which surrounds the infarct core. Intravenous thrombolysis remains the fundamental treatment worldwide, though not ideal for various restrictions and complications, limiting to 10% or less the percentage of patients treated within the appropriate time window.

Neuroprotection is an alternative or adjunct approach to thrombolysis, targeting cerebral parenchyma in the acute ischaemic phase. Furthermore, neurorepair attempts to restore neuronal function in the after-stroke phase in those patients (treated or untreated) with significant impairment.

In the past decades, the efficacy and safety of numerous candidate neuroprotective agents were shown in various animal stroke models. However, in clinical trials, promising pre-clinical studies have not been translated into positive outcomes. Our review will analyse the possible reasons for this failure and the new approaches and recommendations to overcome it, as well as novel strategies targeting additional events in ischaemia cascade. The combination of thrombolysis with pharmacological and non-pharmacological neuroprotective approaches has also been tested. Finally, the neurorepair strategy will be described with special emphasis on the role of cell-based therapies and ischaemic conditioning.

Hopefully, the future therapy of ischaemic stroke will encompass a combination of neuroprotection (to stabilise penumbra), thrombolysis, antithrombotics (for secondary prevention) and neurorepair based on cell therapy plus rehabilitation.