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Uncoupling protein-2 prevents neuronal death and diminishes brain dysfunction after stroke and brain trauma
It is proposed that UCP-2 is an inducible protein that is neuroprotective by activating cellular redox signaling or by inducing mild mitochondrial uncoupling that prevents the release of apoptogenic proteins.
Models for studying long‐term recovery following forebrain ischemia in the rat. 2. A 2‐vessel occlusion model
- Maj-lis Smith, G. Béndek, N. Dahlgren, I. Rosén, T. Wieloch, B. Siesjö
- MedicineActa neurologica Scandinavica
- 1 June 1984
By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long‐term recovery studies.
Mechanisms of neural plasticity following brain injury
Cyclosporin A, But Not FK 506, Protects Mitochondria and Neurons against Hypoglycemic Damage and Implicates the Mitochondrial Permeability Transition in Cell Death
- H. Friberg, M. Ferrand-Drake, F. Bengtsson, A. Halestrap, T. Wieloch
- Biology, MedicineThe Journal of Neuroscience
- 15 July 1998
It is concluded that CsA treatment during hypoglycemic coma inhibits the mitochondrial permeability transition (MPT) and reduces damage and that mitochondria and the MPT are likely to be involved in the development of Hypoglycemic brain damage in the rat.
Structural and Functional Damage Sustained by Mitochondria after Traumatic Brain Injury in the Rat: Evidence for Differentially Sensitive Populations in the Cortex and Hippocampus
- J. Lifshitz, H. Friberg, T. Mcintosh
- BiologyJournal of cerebral blood flow and metabolism…
- 1 February 2003
A proposed mitochondrial population model synthesizes data and suggests that cortical mitochondria may be depleted after TBI, with a physically smaller, MPT-regulated population remaining.
Hypoglycemia-induced neuronal damage prevented by an N-methyl-D-aspartate antagonist.
- T. Wieloch
- 8 November 1985
The results suggest that hypoglycemic neuronal damage is induced by NMDA receptor agonists, such as the excitatory amino acids or related compounds.
Mitochondrial permeability transition in acute neurodegeneration.
Mitochondrial damage and dysfunction in traumatic brain injury.
Death-associated Protein Kinase Is Activated by Dephosphorylation in Response to Cerebral Ischemia*
- M. Shamloo, L. Soriano, T. Wieloch, K. Nikolich, R. Urfer, D. Oksenberg
- Biology, ChemistryJournal of Biological Chemistry
- 23 December 2005
Results indicate that DAPK plays a key role in mediating ischemic neuronal injury by being activated by NMDA receptor-mediated calcium flux, activation of calcineurin, and subsequent D APK dephosphorylation.
Novel pharmacologic strategies in the treatment of experimental traumatic brain injury: 1998.
A compendium of recent studies suggesting that modification of post-traumatic neurochemical and cellular events with targeted pharmacotherapy can promote functional recovery following traumatic injury to the central nervous system is presented.