Neuroprotection for ischaemic stroke: Current status and challenges

Moretti, Antonio; Ferrari, Francesca; Villa, R. F.

doi:10.1016/j.pharmthera.2014.09.003

Cited by 208 publications

(146 citation statements)

References 193 publications

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“…The current therapy can restore cerebral blood flow within a narrow time window to prevent damage to the Bpenumbra^area, which surrounds the infarct core [40]. In order to increase the therapeutic time window, neuroprotection is an alternative or adjunct approach to thrombolysis, targeting the cerebral parenchyma in the acute ischemic phase [41]. The neuroprotective effects of the nucleoside GUO have been demonstrated after systemic administration in ischemia models by our and other groups [11][12][13][14][15].…”

Section: Discussionmentioning

confidence: 98%

Intranasal guanosine administration presents a wide therapeutic time window to reduce brain damage induced by permanent ischemia in rats

Ramos

Müller

Rocha

et al. 2015

Purinergic Signalling

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In addition to its intracellular roles, the nucleoside guanosine (GUO) also has extracellular effects that identify it as a putative neuromodulator signaling molecule in the central nervous system. Indeed, GUO can modulate glutamatergic neurotransmission, and it can promote neuroprotective effects in animal models involving glutamate neurotoxicity, which is the case in brain ischemia. In the present study, we aimed to investigate a new in vivo GUO administration route (intranasal, IN) to determine putative improvement of GUO neuroprotective effects against an experimental model of permanent focal cerebral ischemia. Initially, we demonstrated that IN [ 3 H] GUO administration reached the brain in a dose-dependent and saturable pattern in as few as 5 min, presenting a higher cerebrospinal GUO level compared with systemic administration. IN GUO treatment started immediately or even 3 h after ischemia onset prevented behavior impairment. The behavior recovery was not correlated to decreased brain infarct volume, but it was correlated to reduced mitochondrial dysfunction in the penumbra area. Therefore, we showed that the IN route is an efficient way to promptly deliver GUO to the CNS and that IN GUO Purinergic Signalling (2016) 12:149-159 DOI 10.1007 Denise Barbosa Ramos and Gabriel Cardozo Muller contributed equally as first authors.Electronic supplementary material The online version of this article (doi:10.1007/s11302-015-9489-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 98%

Intranasal guanosine administration presents a wide therapeutic time window to reduce brain damage induced by permanent ischemia in rats

Ramos

Müller

Rocha

et al. 2015

Purinergic Signalling

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“…However, owing to its narrow time window, < 5 % of stroke patients receive this treatment. Although the use of mechanic thrombectomy is helping to expand this window, it is still imperative to pursue the search of new therapeutic targets amenable to pharmacological manipulation for stroke patients [5]. Traumatic brain injury (TBI) is another important focal form of acquired brain injury that occurs when a sudden trauma damages the brain.…”

Section: Cannabinoids and Acute Brain Damage: Stroke And Brain Traumamentioning

confidence: 99%

Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications

2015

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Cannabinoids form a singular family of plantderived compounds (phytocannabinoids), endogenous signaling lipids (endocannabinoids), and synthetic derivatives with multiple biological effects and therapeutic applications in the central and peripheral nervous systems. One of these properties is the regulation of neuronal homeostasis and survival, which is the result of the combination of a myriad of effects addressed to preserve, rescue, repair, and/or replace neurons, and also glial cells against multiple insults that may potentially damage these cells. These effects are facilitated by the location of specific targets for the action of these compounds (e.g., cannabinoid type 1 and 2 receptors, endocannabinoid inactivating enzymes, and nonendocannabinoid targets) in key cellular substrates (e.g., neurons, glial cells, and neural progenitor cells). This potential is promising for acute and chronic neurodegenerative pathological conditions. In this review, we will collect all experimental evidence, mainly obtained at the preclinical level, supporting that different cannabinoid compounds may be neuroprotective in adult and neonatal ischemia, brain trauma, Alzheimer's disease, Parkinson's disease, Huntington's chorea, and amyotrophic lateral sclerosis. This increasing experimental evidence demands a prompt clinical validation of cannabinoid-based medicines for the treatment of all these disorders, which, at present, lack efficacious treatments for delaying/arresting disease progression, despite the fact that the few clinical trials conducted so far with these medicines have failed to demonstrate beneficial effects.

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“…Moreover, each hour the brain loses as many neurons as it does in almost 3.6 years of simple ageing 9 . Therefore, the primary aim of treatments is to restore cerebral blood flow (CBF) as soon as possible, inhibiting the spreading of irreversible injury due to the expansion of the infract core into the ischemic penumbra.…”

Section: Treatment Of Acute Ischemic Strokementioning

confidence: 99%

Pharmacological Treatment of Acute Ischemic Stroke: A Review

Nayak¹,

Kumar²,

Sah³

2017

Int. Res. J. Pharm.

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Stroke is severe neurological disorder characterized by interruption of blood circulation into the brain and the leading cause of serious long-term disability. The central goal of therapy in ischemic stroke is to preserve tissue in the ischemic penumbra, where perfusion is decreased but sufficient to stave off infarction. Therefore, the fundamental treatment of AIS relies on prompt recanalisation and reperfusion of the threatened, but potentially salvageable, ischemic penumbra. Intravenous (iv) thrombolysis with recombinant tissue plasminogen activator (rtPA) remains the current strategy. However, other thrombolysis is underused, owing to various exclusion criteria that limit the number of treated patients. Other thrombolytics are under investigation. Intra-arterial thrombolysis and mechanical thrombectomy devices is also increasingly applied. This review analyses the current status and the problem of the pharmacological treatment of acute ischemic stroke.

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Neuroprotection for ischaemic stroke: Current status and challenges

Cited by 208 publications

References 193 publications

Intranasal guanosine administration presents a wide therapeutic time window to reduce brain damage induced by permanent ischemia in rats

Intranasal guanosine administration presents a wide therapeutic time window to reduce brain damage induced by permanent ischemia in rats

Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications

Pharmacological Treatment of Acute Ischemic Stroke: A Review

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