Increased oxidative protein and DNA damage but decreased stress response in the aged brain following experimental stroke

Li, Songlin; Zheng, Jian; Carmichael, S. Thomas

doi:10.1016/j.nbd.2004.12.014

Cited by 42 publications

(30 citation statements)

References 76 publications

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“…The precise mapping of tissue microenvironments after stroke within a defined cortical structure has allowed comparison of mechanisms of stroke damage between aged and young adults, and identified reduced neuroprotective and cellular stress responses in the aged brain. 132 A similar model has been developed in the mouse (FIG. 2).…”

Section: Animal Models Of Neural Repair In Strokementioning

confidence: 99%

Rodent models of focal stroke: Size, mechanism, and purpose

2005

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Summary: Rodent stroke models provide the experimental backbone for the in vivo determination of the mechanisms of cell death and neural repair, and for the initial testing of neuroprotective compounds. Less than 10 rodent models of focal stroke are routinely used in experimental study. These vary widely in their ability to model the human disease, and in their application to the study of cell death or neural repair. Many rodent focal stroke models produce large infarcts that more closely resemble malignant and fatal human infarction than the average sized human stroke. This review focuses on the mechanisms of ischemic damage in rat and mouse stroke models, the relative size of stroke generated in each model, and the purpose with which focal stroke models are applied to the study of ischemic cell death and to neural repair after stroke.

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Section: Animal Models Of Neural Repair In Strokementioning

confidence: 99%

Rodent models of focal stroke: Size, mechanism, and purpose

2005

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“…The other mediator of reperfusion injury, oxidative stress, results from an imbalance between the production and neutralization of reactive oxygen species. Reactive oxygen species have been shown to increase neuronal death and infarct volume (Bemeur et al, 2005(Bemeur et al, , 2007Li et al, 2005;Muralikrishna and Hatcher, 2006;Suh et al, 2008). In experimental ischemic stroke, hyperglycemia increases the production of reactive oxygen species through the activation of protein kinase C and through increased NADP production, thus promoting oxidative stress.…”

Section: How Does Hyperglycemia Affect Outcome After Aneurysmal Subarmentioning

confidence: 99%

Hyperglycemia in Aneurysmal Subarachnoid Hemorrhage: A Potentially Modifiable Risk Factor for Poor Outcome

Kruyt

Biessels

DeVries

et al. 2010

J Cereb Blood Flow Metab

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Hyperglycemia after aneurysmal subarachnoid hemorrhage (aSAH) occurs frequently and is associated with delayed cerebral ischemia (DCI) and poor clinical outcome. In this review, we highlight the mechanisms that cause hyperglycemia after aSAH, and we discuss how hyperglycemia may contribute to poor clinical outcome in these patients. As hyperglycemia is potentially modifiable with intensive insulin therapy (IIT), we systematically reviewed the literature on IIT in aSAH patients. In these patients, IIT seems to be difficult to achieve in terms of lowering blood glucose levels substantially without an increased risk of (serious) hypoglycemia. Therefore, before initiating a large-scale randomized trial to investigate the clinical benefit of IIT, phase II studies, possibly with the help of cerebral blood glucose monitoring by microdialysis, will first have to improve this therapy in terms of both safety and adequacy.

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“…The experiments are usually carried out on neonates, young adults from 3-6 months old or, occasionally, on elderly 2-year-old rats. The CNS of a neonate may allow far greater opportunity for molecular and morphologic adaptations than can evolve in an adult, although some models suggest that older age does not exclude the possibility of repair manipulations (Li et al, 2005;Markus et al, 2005).…”

Section: Differences In Rodent Modelsmentioning

confidence: 99%

Curiosity and cure: Translational research strategies for neural repair‐mediated rehabilitation

Dobkin

2007

Developmental Neurobiology

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Clinicians who seek interventions for neural repair in patients with paralysis and other impairments may extrapolate the results of cell culture and rodent experiments into the framework of a preclinical study. These experiments, however, must be interpreted within the context of the model and the highly constrained hypothesis and manipulation being tested. Rodent models of repair for stroke and spinal cord injury offer examples of potential pitfalls in the interpretation of results from developmental gene activation, transgenic mice, endogeneous neurogenesis, cellular transplantation, axon regeneration and remyelination, dendritic proliferation, activity-dependent adaptations, skills learning, and behavioral testing. Preclinical experiments that inform the design of human trials ideally include a lesion of etiology, volume and location that reflects the human disease; examine changes induced by injury and by repair procedures both near and remote from the lesion; distinguish between reactive molecular and histologic changes versus changes critical to repair cascades; employ explicit training paradigms for the reacquisition of testable skills; correlate morphologic and physiologic measures of repair with behavioral measures of task reacquisition; reproduce key results in more than one laboratory, in different strains or species of rodent, and in a larger mammal; and generalize the results across several disease models, such as axonal regeneration in a stroke and spinal cord injury platform. Collaborations between basic and clinical scientists in the development of translational animal models of injury and repair can propel experiments for ethical bench-to-bedside therapies to augment the rehabilitation of disabled patients.

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Increased oxidative protein and DNA damage but decreased stress response in the aged brain following experimental stroke

Cited by 42 publications

References 76 publications

Rodent models of focal stroke: Size, mechanism, and purpose

Rodent models of focal stroke: Size, mechanism, and purpose

Hyperglycemia in Aneurysmal Subarachnoid Hemorrhage: A Potentially Modifiable Risk Factor for Poor Outcome

Curiosity and cure: Translational research strategies for neural repair‐mediated rehabilitation

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