Abstract
Acute neurodegeneration in man is encountered during and following stroke, transient cardiac arrest, brain trauma, insulin-induced hypoglycemia and status epilepticus. All these severe clinical conditions are characterized by neuronal calcium overload, aberrant cell signaling, generation of free radicals and elevation of cellular free fatty acids, conditions that favor activation of the mitochondrial permeability transition pore (mtPTP). Cyclosporin A (CsA) and its analog N-methyl-valine-4-cyclosporin A (MeValCsA) are potent blockers of the mtPTP and protect against neuronal death following excitotoxicity and oxygen glucose deprivation. Also, CsA and MeValCsA diminish cell death following cerebral ischemia, trauma, and hypoglycemia. Here we present data that strongly imply the mtPT in acute neurodegeneration in vivo. Compounds that readily pass the blood-brain-barrier (BBB) and block the mtPT may be neuroprotective in stroke.
| Original language | English |
|---|---|
| Pages (from-to) | 241-250 |
| Journal | Biochimie |
| Volume | 84 |
| Issue number | 2-3 |
| Publication status | Published - 2002 |
Bibliographical note
The information about affiliations in this record was updated in December 2015.The record was previously connected to the following departments: Experimental Brain Research (0131000120), Anaesthesiology and Intensive Care (013230022), Neurosurgery (013026000)
Subject classification (UKÄ)
- Biological Sciences