A review of current imaging methods used in stroke research

Wey, Hsiao Ying; Desai, Virendra R.; Duong, Timothy Q.

doi:10.1179/1743132813y.0000000250

Cited by 29 publications

(24 citation statements)

References 112 publications

(119 reference statements)

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“…Stroke was induced in conscious, spontaneously hypertensive rats (SHRs) by titrating endothelin-1 (ET-1) above the right middle cerebral artery (MCA) via an indwelling cannula to cause vessel occlusion and evoke stroke-induced behavior (14). This vasoconstrictive stroke model more closely resembles human stroke than mechanical occlusion models (3). A single small dose of Hi1a (2 ng/kg) administered i.c.v.…”

Section: Reversible (Fig 3fmentioning

confidence: 99%

“…stroke | acid-sensing ion channel 1a | venom peptide | neuroprotection | ischemia M ost strokes (>85%) are ischemic (1)(2)(3), and the disruption of blood flow that occurs during cerebral ischemia leads to neuronal damage in localized vascular territories within a few minutes (4). Whether blood flow is completely or partially impeded defines two distinct regions of tissue damage, known as the core and penumbral (peri-infarct) zones, respectively (1)(2)(3)5). The core tissue exposed to the most dramatic reduction in blood flow is mortally injured and thought to undergo irreversible necrotic cell death (2).…”

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confidence: 99%

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Potent neuroprotection after stroke afforded by a double-knot spider-venom peptide that inhibits acid-sensing ion channel 1a

Chassagnon

McCarthy

Chin

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

193

271

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Stroke is the second-leading cause of death worldwide, yet there are no drugs available to protect the brain from stroke-induced neuronal injury. Acid-sensing ion channel 1a (ASIC1a) is the primary acid sensor in mammalian brain and a key mediator of acidosis-induced neuronal damage following cerebral ischemia. Genetic ablation and selective pharmacologic inhibition of ASIC1a reduces neuronal death following ischemic stroke in rodents. Here, we demonstrate that Hi1a, a disulfide-rich spider venom peptide, is highly neuroprotective in a focal model of ischemic stroke. Nuclear magnetic resonance structural studies reveal that Hi1a comprises two homologous inhibitor cystine knot domains separated by a short, structurally well-defined linker. In contrast with known ASIC1a inhibitors, Hi1a incompletely inhibits ASIC1a activation in a pH-independent and slowly reversible manner. Whole-cell, macropatch, and single-channel electrophysiological recordings indicate that Hi1a binds to and stabilizes the closed state of the channel, thereby impeding the transition into a conducting state. Intracerebroventricular administration to rats of a single small dose of Hi1a (2 ng/kg) up to 8 h after stroke induction by occlusion of the middle cerebral artery markedly reduced infarct size, and this correlated with improved neurological and motor function, as well as with preservation of neuronal architecture. Thus, Hi1a is a powerful pharmacological tool for probing the role of ASIC1a in acid-mediated neuronal injury and various neurological disorders, and a promising lead for the development of therapeutics to protect the brain from ischemic injury.

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Section: Reversible (Fig 3fmentioning

confidence: 99%

mentioning

confidence: 99%

Potent neuroprotection after stroke afforded by a double-knot spider-venom peptide that inhibits acid-sensing ion channel 1a

Chassagnon

McCarthy

Chin

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

193

271

View full text Add to dashboard Cite

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“…When blood flow is < 10 mL/100 g/min, the tissue loses ionic homeostasis and forms the infarct core (Hakim 1998). Neuroimaging techniques have provided a method to anatomically distinguish between the core and penumbra (Wey et al 2013). The method of choice to discriminate between these two regions is positron emission tomography/ single photon emission CT, which measures cerebral blood flow and glucose metabolism.…”

Section: Core Vs Penumbramentioning

confidence: 99%

Chloride co‐transporters as possible therapeutic targets for stroke

Baudel

Poole

Darlison

2016

Journal of Neurochemistry

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Stroke is one of the major causes of death and disability worldwide. The major type of stroke is an ischaemic one, which is caused by a blockage that interrupts blood flow to the brain. There are currently very few pharmacological strategies to reduce the damage and social burden triggered by this pathology. The harm caused by the interruption of blood flow to the brain unfolds in the subsequent hours and days, so it is critical to identify new therapeutic targets that could reduce neuronal death associated with the spread of the damage. Here, we review some of the key molecular mechanisms involved in the progression of neuronal death, focusing on some new and promising studies. In particular, we focus on the potential of the chloride co-transporter (CCC) family of proteins, mediators of the GABAergic response, both during the early and later stages of stroke, to promote neuroprotection and recovery. Different studies of CCCs during the chronic and recovery phases post-stroke reveal the importance of timing when considering CCCs as potential neuroprotective and/or neuromodulator targets. The molecular regulatory mechanisms of the two main neuronal CCCs, NKCC1 and KCC2, are further discussed as an indirect approach for promoting neuroprotection and neurorehabilitation following an ischaemic insult. Finally, we mention the likely importance of combining different strategies in order to achieve more effective therapies.

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“…For example, limited spatial resolution of MR images in the rodent brain has traditionally precluded the measurement of midline shift (MLS) from clinically relevant structures such as the septum pellucidum [36,37] and necessitated measurement from the third ventricle [38]. Additionally, unlike the lissencephalic rodent brain, the gyrencephalic brains of pigs and humans have increased heterogeneity in blood flow due to collateral circulation and differences in gray and white matter composition that are uniquely affected by stroke, resulting in differential rates of penumbra evolution [39]. These neuroanatomical similarities allow for a more faithful representation of clinical stroke progression and therefore greater confidence in the translational potential of identified predictive MRI parameters.…”

Section: Introductionmentioning

confidence: 99%

Neural Stem Cell Extracellular Vesicles Disrupt Midline Shift Predictive Outcomes in Porcine Ischemic Stroke Model

Spellicy

Kaiser

Bowler

et al. 2019

Transl. Stroke Res.

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Magnetic resonance imaging (MRI) is a clinically relevant non-invasive imaging tool commonly utilized to assess stroke progression in real time. This study investigated the utility of MRI as a predictive measure of clinical and functional outcomes when a stroke intervention is withheld or provided, in order to identify biomarkers for stroke functional outcome under these conditions. Fifteen MRI and ninety functional parameters were measured in a middle cerebral artery occlusion (MCAO) porcine ischemic stroke model. Multiparametric analysis of correlations between MRI measurements and functional outcome was conducted. Acute axial and coronal midline shift (MLS) at 24 h post-stroke were associated with decreased survival and recovery measured by modified Rankin scale (mRS) and were significantly correlated with 52 measured acute (day 1 post) and chronic (day 84 post) gait and behavior impairments in non-treated stroked animals. These results suggest that MLS may be an important non-invasive biomarker that can be used to predict patient outcomes and prognosis as well as guide therapeutic intervention and rehabilitation in non-treated animals and potentially human patients that do not receive interventional treatments. Neural stem cell-derived extracellular vesicle (NSC EV) was a disruptive therapy because NSC EVadministration post-stroke disrupted MLS correlations observed in non-treated stroked animals. MLS was not associated with survival and functional outcomes in NSC EV-treated animals. In contrast to untreated animals, NSC EVs improved stroked animal outcomes regardless of MLS severity.

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A review of current imaging methods used in stroke research

Cited by 29 publications

References 112 publications

Potent neuroprotection after stroke afforded by a double-knot spider-venom peptide that inhibits acid-sensing ion channel 1a

Potent neuroprotection after stroke afforded by a double-knot spider-venom peptide that inhibits acid-sensing ion channel 1a

Chloride co‐transporters as possible therapeutic targets for stroke

Neural Stem Cell Extracellular Vesicles Disrupt Midline Shift Predictive Outcomes in Porcine Ischemic Stroke Model

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