Mitochondrial control of neuron death and its role in neurodegenerative disorders

Jordán, Joaquı́n; Ceña, Valentı́n; Prehn, Jochen H M

doi:10.1007/bf03179878

Cited by 97 publications

(59 citation statements)

References 87 publications

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“…Mitochondria are considered the main link between cellular stress signals and the execution of neuronal programmed cell death (34). Conditions during reperfusion are likely to be conducive to the induction of the permeability transition in mitochondria.…”

Section: Fig 3 Ischemia Results In Rapid Loss Of High-energy Phosphmentioning

confidence: 99%

Stroke pathophysiology: management challenges and new treatment advances

Jordán

Ikuta

García-García

et al. 2007

J. Physiol. Biochem.

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J. JORDÁN, I. IKUTA, J. GARCÍA-GARCÍA, S. CALLEJA and T. SEGURA. Stroke pathophysiology: Management challenges and new treatment advances (minireview). J. Physiol. Biochem., 63 (3), 261-278, 2007. Stroke is the second leading cause of death and the first cause of lost disabilityadjusted years in developed countries. During the past decade, new developments in thrombolytic therapy have led to the implementation of emergency intervention protocols for the treatment of ischemic stroke, replacing the widespread sense of therapeutic nihilism in the past. Treatment with rtPA has shown to be effective within the first 3 hours following stroke onset and the FDA and the European Medical Agency (EMEA) have approved its use. Acknowledging the urgency and intricacies of stroke, Stroke Units allow the monitoring of physiological parameters in the acute phase of stroke and are considered an important management tool that can significantly improve the quality of care provided to the patient. The concept of neuroprotective therapy for acute ischemic stroke to salvage tissue at risk and improve functional outcome is based on sound scientific principles and extensive preclinical animal studies demonstrating efficacy. However, most neuroprotective drugs in clinical trials have failed, possibly due to inadequate preclinical testing or flawed clinical development programs. Several new treatment strategies are under development and are being tested. This review is directed at understanding the management of acute ischemic stroke pathophysiology. We address the management challenges and new treatment advances by integrating the knowledge of possible pharmacological targets for acute ischemic stroke. We hope to shed new light upon the controversy surrounding the management of acute ischemic stroke in an attempt to elucidate why failed clinical trials continue to occur despite promising neuroprotective preclinical studies.

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Section: Fig 3 Ischemia Results In Rapid Loss Of High-energy Phosphmentioning

confidence: 99%

Stroke pathophysiology: management challenges and new treatment advances

Jordán

Ikuta

García-García

et al. 2007

J. Physiol. Biochem.

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“…Evidence for the occurrence of this permeability transition in situ has been gathered from astrocytes, neurons and a plethora of nonneuronal cells (Dubinsky and Levi, 1998;Jordan et al, 2003). When neuronal cytosolic Ca 2+ is elevated with an excitotoxic dose of glutamate, mitochondria depolarize in a manner that may or may not be sensitive to inhibitors of the permeability transition (Brustovetsky and Dubinsky, 2000b;Reynolds, 1999).…”

Section: Er Stressmentioning

confidence: 99%

“…Mitochondria act as a transient Ca 2+ sink during rapid events that increase cytosolic Ca 2+ , such as the neuronal action potential , and during longer lasting events associated with Ca 2+ waves (Landgraf era/., 2004 depolarization, swelling, and an eventual inability of mitochondria to sequester the calcium. Evidence for the occurrence of this permeability transition in situ has been gathered from astrocytes, neurons, and a plethora of nonneuronal cells (Dubinsky and Levi, 1998;Jordan et al, 2003;. When neuronal cytosolic Ca 2+ is elevated with an excitotoxic dose of glutamate, mitochondria depolarize in a manner that may or may not be sensitive to inhibitors of the permeability transition (Brustovetsky and Dubinsky, 2000b;Reynolds, 1999).…”

Section: Protective Roles Of Cns Mitochondriamentioning

confidence: 99%

Perioperative Neuroprotection Symposium

Fiskum¹

2004

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Public reporting burden for this collection of information is estimated to average 1 hour par the data needed, and completing and reviewing this collection of information. Send conranls reducing this burden to Washington Headquarters Services. Directorate for Information Operations Management and Budget, Paperwork Reduction Protect (0704-01681. Washington, DC 20803Indudkig the «ma for reviewing instructions, searching existing data sources, gathering and maintaining tMs burden estimate or any other aspect of this ooHecMon of information, including suggestions for 1218 Jefferson Davis Highway, Suite 1204, Arttngton, VA 22202-4302, and to the Office of AGENCY USE ONLY (Leave blank) REPORT DATE June 2004 REPORT TYPE AND DATES COVERED Final Proceedings (13 Sep 03-22 May 04) TITLE AND SUBTITLE Perioperative Neuroprotection Symposium AUTHOR(S)Gary Fiskum, Ph.D. S. FUNDING NUMBERS DAMD17-03-1-0500 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)University of Maryland, Baltimore Baltimore, MD 21201 E-Mail: gfisk001@umaryland.edu PERFORMING ORGANIZATION REPORT NUMBER SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSORING / MONITORING AGENCY REPORT NUMBER SUPPLEMENTARY NOTESOriginal contains color plates: ALL DTIC reproductions will be in black and white 12a. DISTRIBUTION / AVAILABILITY STATEMENT Approved for Public Release; Distribution Unlimited 12b. DISTRIBUTION CODE A-TRACT IMaiiliwyiH 200 VVwW)The Perioperative Neuroprotection Symposium was held on April 16-19 in Ft. Lauderdale, Fl. The meeting was attended by approximately 140 registrant». Twenty four invited speakers made presentations in five sessions. An additional 40 poster presentations were^available for discussion throughout the meeting. Each participant received a symposium abstract book that included mini-reviews from each of the speakers and the short abstracts from the posters. The speakers also submitted formal manuscripts for peer-reviewed publication.Five of the poster presenters were also invited to submit short research manuscripts. Mitochondria and Neuroprotection Symposium April [16][17][18][19] 2004 Albert Lester Lehninger February 17,1917-March4,1986 Albert Lehninger was born in Bridgeport, Connecticut and received a B.A. in English from Wesleyan University in 1939. He received his Ph.D. in Physiological Chemistry from the University of Wisconsin in 1942. Lehninger stayed on at the Univ. of Wisconsin as an Instructor until 1945, when he was appointed Assistant Professor of Biochemistry and Surgery at the University of Chicago. At this juncture he had published 11 research articles. From 1945From -1952, he published an additional 33 articles. These studies included the discovery that fatty acid oxidation, ketone body metabolism, and the TCA cycle occur in the mitochondrion, some of the first investigations employing isolation of this organelle (see e.g., JBC1949 and 1950). Thus, while Lehninger was a chemist at heart, he was one of the founding father...

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“…This process is usually limited by endogenous buffers including proteins like calbindin and organelles like mitochondria. However, if mitochondria take up too much Ca2+, they favor the delayed rise in [Ca2+]cyt [6] as well as the opening of the so-called mitochondrial [AU1] [AU2] permeability transition pore, a not well understood phenomenon that precedes release of cytochrome c and other pro-apoptotic factors culminating in apoptosis [7]. Therefore, changes in neuronal [Ca2+]cyt are critical in neuron apoptosis and cell death.…”

Section: Introductionmentioning

confidence: 99%