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Medical Forum / General / Alternative / June 2008Brain Iron After Stroke
Stroke. 2008;39:1541. MRI Detection of Secondary Damage After Stroke Chronic Iron Accumulation in the Thalamus of the Rat Brain Carles Justicia, PhD; Pedro Ramos-Cabrer, PhD Mathias Hoehn, PhD From the In-vivo-NMR-Laboratory (C.J., P.R.-C., M.H.), Max Planck Institute for Neurological Research, Cologne, Germany; Brain Ischemia and Neurodegeneration (C.J.), IIBB-CSIC, IDIBAPS, Barcelona, Spain; and Clinical Neurosciences Research Laboratory (P.R.-C.), Hospital Clínico Universitario, Santiago de Compostela, Spain. Correspondence to Prof Dr Mathias Hoehn, In-vivo-NMR-Laboratory, Max- Planck-Institute for Neurological Research, Gleuelerstrasse 50, D-50931 Cologne, Germany. E-mail mathias@nf.mpg.de Background and Purpose— Iron plays a central role in many metabolic processes. Under certain pathological situations it accumulates, producing negative effects such as increasing damage by oxidative stress. The present study examined long-term iron accumulation in a stroke model with secondary degeneration, using MRI and histological techniques. Methods— Male Wistar rats (n=22) were subjected to 60 minutes MCA occlusion. MR images (T2- and T2*-weighted) were obtained weekly between weeks 1 and 7 after reperfusion, and at weeks 10, 14, 20, and 24. Histological iron detection and immunohistochemical examination for different markers (NeuN, GFAP, OX-42, HO-1, and APP) were performed at the 3 survival time points (3, 7, and 24 weeks). Results— Infarcts affecting MCA territory were evident on T2-weighted imaging, and all animals showed deficits on behavioral tests. In the thalamus, T2 hyperintensity was detected 3 weeks after stroke, and disappeared around week 7 when T2*-weighted images showed a marked hypointensity in that area. Histology revealed neuronal loss in the thalamus, accompanied by strong microglial reactivity and microglial HO-1 expression. APP deposits were detected in the thalamus from week 3 on and persisted until week 24. Iron storage was detected in microglia at week 3, in the parenchyma at week 7, and around APP deposits at week 24. Conclusions— T2*-weighted MRI allows the detection of secondary damage in the thalamus after MCAO. Iron accumulation in the thalamus is mediated by HO-1 expression in reactive microglia. Key Words: transient cerebral ischemia • thalamus • magnetic resonance imaging • iron • heme-oxigenase-1 Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk On Jun 16, 3:55 pm, ironjustice <teamtan...@hotmail.com> wrote: Iron accumulation in the thalamus << "Hemoglobin is a potent slowly-acting neurotoxin" J Neurotrauma. 2003 Jan;20(1):111-20. Links Delayed treatment of hemoglobin neurotoxicity. Regan RF, Rogers B. Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. Raymond.F.Regan@mail.tju.edu Hemoglobin is an oxidative neurotoxin that may contribute to cell injury after CNS trauma and hemorrhagic stroke. Prior studies have demonstrated that concomitant treatment with iron- chelating antioxidants prevents its neurotoxicity. However, the efficacy of these agents when applied hours after hemoglobin has not been determined, and is the subject of the present investigation. Consistent with prior observations, an increase in reactive oxygen species generation, detected by 2',7'-dichlorofluorescin oxidation, was observed when mixed neuronal/astrocyte cultures prepared from mouse cortex were exposed to hemoglobin alone. However, this oxidative stress developed slowly. A significant increase in the dichlorofluorescein signal compared with control, untreated cultures was not observed until four hours after addition of hemoglobin, and was followed by loss of membrane integrity and propidium iodide staining. Treating cultures with the 21- aminosteroid U74500A or the ferric iron chelator deferoxamine four hours after initiating hemoglobin treatment markedly attenuated reactive oxygen species production within 2 h. Continuous exposure to 5 micro M hemoglobin for 24 h resulted in death of about three-quarters of neurons, without injuring astrocytes. Most neuronal loss was prevented by concomitant treatment with U74500A; its effect was not significantly attenuated if treatment was delayed for 2-4 h, and it still prevented over half of neuronal death if treatment was delayed for 8 h. Similar neuroprotection was produced by delayed treatment with deferoxamine or the lipid-soluble iron chelator phenanthroline. None of these agents had any effect on neuronal death when added to cultures 12 h after hemoglobin. These results suggest that hemoglobin is a potent but slowly-acting neurotoxin. The delayed onset of hemoglobin neurotoxicity may make it an attractive target for therapeutic intervention. PMID: 12614593 [PubMed - indexed for MEDLINE] Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9f > Stroke. 2008;39:1541. > MRI Detection of Secondary Damage AfterStroke [quoted text clipped - 50 lines] > > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk |
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