Abstract
Stroke is one of the major contributors of mortality and morbidity worldwide. It results due to sudden blockade of blood flow into the brain thereby leading to breakdown of hemodynam - ic, biochemical and metabolic processes in the affected territory. These alterations are dependent on the severity and duration of the ischemia and modulated by pathophysiologic mechanisms that in- clude excitotoxicity, calcium overload, oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, acidosis, inflammation and activation of cell death pathways. As there is no current therapy to minimize post-stroke brain damage and most of the clinical trials failed, it is impera- tive to design novel approaches including glutamate receptor antagonists, free radical scavengers/ anti-oxidants, anti-inflammatory and anti-apoptotic agents, and growth factors to prevent the pro - gression and increase the plasticity of neuronal damage after stroke. Additionally, rigorous in vitro and in vivo animal testing of potential drugs molecules is necessary to reduce the failure of clinical trials.
Highlights
Abstract | Stroke is one of the major contributors of mortality and morbidity worldwide
The core region is surrounded by a zone of borderline ischemic tissue called ischemic penumbra with blood flow ranging from 7-17mL/100g/ min (Baron, 1999)
Penumbra can be identified by multitracer positron emission tomography or perfusion-weighted imaging/diffusion-weighted imaging mismatch in acute stroke (Reid et al, 2012), and can be described in molecular terms, such as changes in heat shock proteins 70, which is selectively induced in response to transient ischemic stroke in the area of decreased blood flow and oxygen delivery (Hata et al, 2000; Sharp et al, 2000)
Summary
It results due to sudden blockade of blood flow into the brain thereby leading to breakdown of hemodynamic, biochemical and metabolic processes in the affected territory. These alterations are dependent on the severity and duration of the ischemia and modulated by pathophysiologic mechanisms that include excitotoxicity, calcium overload, oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, acidosis, inflammation and activation of cell death pathways. As there is no current therapy to minimize post-stroke brain damage and most of the clinical trials failed, it is imperative to design novel approaches including glutamate receptor antagonists, free radical scavengers/ anti-oxidants, anti-inflammatory and anti-apoptotic agents, and growth factors to prevent the progression and increase the plasticity of neuronal damage after stroke.
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