Neuronal death in brain infarcts in man

Love, Seth; Barber, Rachel; Wilcock, Gordon

doi:10.1046/j.1365-2990.2000.00218.x

Cited by 124 publications

(58 citation statements)

References 45 publications

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“…An analysis of autopsy samples of human stroke patients failed to reveal an apoptotic morphology [116] . The biochemical events that lead to neuronal cell death in the penumbra are generally more subtle and there is much debate as to whether this type of cell death represents a classical form of caspase-3-mediated apoptosis.…”

Section: Caspase-3 and Active Caspase-3mentioning

confidence: 99%

Pathophysiology of Acute Ischaemic Stroke: An Analysis of Common Signalling Mechanisms and Identification of New Molecular Targets

et al. 2006

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Stroke continues to be a major cause of death and disability. The currently available therapies have proven to be highly unsatisfactory (except thrombolysis) and attempts are being made to identify and characterize signalling proteins which could be exploited to design novel therapeutic modalities. The pathophysiology of stroke is a complex process. Delaying interventions from the first hours to days or even weeks following blood vessel occlusion may lead to worsening or impairment of recovery in later stages. The objective of this review is to critically evaluate the major mechanisms underlying stroke pathophysiology, especially the role of cell signalling in excitotoxicity, inflammation, apoptosis, neuroprotection and angiogenesis, and highlight potential novel targets for drug discovery.

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Section: Caspase-3 and Active Caspase-3mentioning

confidence: 99%

Pathophysiology of Acute Ischaemic Stroke: An Analysis of Common Signalling Mechanisms and Identification of New Molecular Targets

et al. 2006

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“…Although most studies have been carried out in animal models, a similar scenario seems to occur in human stroke [40] (fig. 1).…”

Section: The Area Around the Core Of The Infarction: The Penumbramentioning

confidence: 99%

Apoptosis: Future Targets for Neuroprotective Strategies

Ferrer

2006

Cerebrovasc Dis

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Focal permanent or transient cerebral artery occlusion produces massive cell death in the central core of the infarction, whereas in the peripheral zone (penumbra) nerve cells are subjected to various determining survival and death signals. Cell death in the core of the infarction and in the adult brain is usually considered a passive phenomenon, although events largely depend on the partial or complete disruption of crucial metabolic pathways. Cell death in the penumbra is currently considered an active process largely dependent on the activation of cell death programs leading to apoptosis. Yet cell death in the penumbra includes apoptosis, necrosis, intermediate and other forms of cell death. A rather simplistic view implies poor prospects regarding cell survival in the core of the infarction and therapeutic expectations in the control of cell death and cell survival in the penumbra. However, the capacity for neuroprotection depends on multiple factors, primarily the use of the appropriate agent, at the appropriate time and during the appropriate interval. Understanding the mechanisms commanding cell death and survival area is as important as delimiting the therapeutic time window and the facility of a drug to effectively impact on specific targets. Moreover, the detrimental effects of homeostasis and the activation of multiple pathways with opposing signals following ischemic stroke indicate that better outcome probably does not depend on a single compound but on several drugs acting in combination at the optimal time in a particular patient.

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“…Caspase-3 is also activated by ischemic injury (9,51), and administration of caspase-3 inhibitors has been shown to decrease the infarction volume (52,53). Similarly, it has been shown that i.v.…”

Section: ϫ7mentioning

confidence: 99%

The neuroprotective effect of pituitary adenylate cyclase-activating polypeptide on cerebellar granule cells is mediated through inhibition of the CED3-related cysteine protease caspase-3/CPP32

Vaudry

Gonzalez

Basille

et al. 2000

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

126

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Caspase-3 knockout mice exhibit thickening of the internal granule cell layer of the cerebellum. Concurrently, it has been shown that intracerebral injection of pituitary adenylate cyclase-activating polypeptide (PACAP) induces a transient increase of the thickness of the cerebellar cortex. In the present study, we have investigated the possible effect of PACAP on caspase activity in cultured cerebellar granule cells from 8-day-old rat.

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Neuronal death in brain infarcts in man

Cited by 124 publications

References 45 publications

Pathophysiology of Acute Ischaemic Stroke: An Analysis of Common Signalling Mechanisms and Identification of New Molecular Targets

Pathophysiology of Acute Ischaemic Stroke: An Analysis of Common Signalling Mechanisms and Identification of New Molecular Targets

Apoptosis: Future Targets for Neuroprotective Strategies

The neuroprotective effect of pituitary adenylate cyclase-activating polypeptide on cerebellar granule cells is mediated through inhibition of the CED3-related cysteine protease caspase-3/CPP32

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