Article citations

    R. K. Sumbria, R. J. Boado, and W. M. Pardridge, “Brain protection from stroke with intravenous TNFα decoy receptor-Trojan horse fusion protein,” Journal of Cerebral Blood Flow & Metabolism, vol. 32, no. 10, pp. 1933–1938, 2012.

has been cited by the following article:

  • TITLE: Influence of Inflammation on Poststroke Plasticity
  • AUTHORS: Monika Liguz-Lecznar,Malgorzata Kossut
  • JOURNAL NAME: Neural Plasticity DOI: 10.1155/2013/258582 Sep 17, 2014
  • ABSTRACT: Age-related brain injuries including stroke are a leading cause of morbidity and mental disability worldwide. Most patients who survive stroke experience some degree of recovery. The restoration of lost functions can be explained by neuronal plasticity, understood as brain ability to reorganize and remodel itself in response to changed environmental requirements. However, stroke triggers a cascade of events which may prevent the normal development of the plastic changes. One of them may be inflammatory response initiated immediately after stroke, which has been found to contribute to neuronal injury. Some recent evidence though has suggested that inflammatory reaction can be also neuroprotective. This paper attempts to discuss the influence of poststroke inflammatory response on brain plasticity and stroke outcome. We also describe the recent anti-inflammatory strategies that have been effective for recovery in experimental stroke. 1. Introduction Ischemic stroke results from two main pathological processes: a loss of oxygen and an interruption of glucose supply to a particular brain region. The collapse of energy provision leads to the dysfunction of ionic pumps, loss of membrane potential, and uncontrolled release of neurotransmitters. The consequence of those processes is the increase of intracellular calcium concentrations that, among many deleterious effects, result in the generation of free radicals, leading to disintegration of cell membranes and subsequent neuronal death in the core of infarction [1]. Necrosis in the center of infarction can start a few minutes after stroke and is followed by peri-infarct depolarizations, excitotoxicity, edema, and oxidative stress [2]. The more delayed processes accompanying stroke are inflammation and apoptosis. They are initiated several hours after ischemic attack and can persist even for several weeks [3]. Although a great progress has been made in understanding the cellular and molecular mechanisms of ischemic tissue damage, the only approved therapy is still thrombolysis achieved by intravenous administration of recombinant tissue plasminogen activator (tPA). Unfortunately, short therapeutic window for this therapy strongly limits the fraction of patient that can benefit from the treatment. Moreover, stroke induces a complex cascade of inflammatory response which contributes to the postischemic damage. The complex nature of phenomena after ischemic event hampers a successful design of effective therapeutic strategies (Figure 1). Figure 1: Acute cerebral ischemia, neuroinflammation, and plasticity.