title: Stroke neuroprotection: targeting mitochondria.
abstract: Stroke is the fourth leading cause of death and the leading cause of long-term disability in the United States. Blood flow deficit results in an expanding infarct core with a time-sensitive peri-infarct penumbra that is considered salvageable and is the primary target for treatment strategies. The only current FDA-approved drug for treating ischemic stroke is recombinant tissue plasminogen activator (rt-PA). However, this treatment is limited to within 4.5 h of stroke onset in a small subset of patients. The goal of this review is to focus on mitochondrial-dependent therapeutic agents that could provide neuroprotection following stroke. Dysfunctional mitochondria are linked to neurodegeneration in many disease processes including stroke. The mechanisms reviewed include: (1) increasing ATP production by purinergic receptor stimulation, (2) decreasing the production of ROS by superoxide dismutase, or (3) increasing antioxidant defenses by methylene blue, and their benefits in providing neuroprotection following a stroke.
authors: Department of Cellular and Structural Biology, University of Texas Health Science Center San Antonio, San Antonio, TX 78229, USA. wattsl@uthscsa.edu.
authors: Lora Talley
authors: LT
authors: Watts
authors: Research Imaging Institute, University of Texas Health Science Center San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA. lloydr@uthscsa.edu.
authors: Reginald
authors: R
authors: Lloyd
authors: School of Medicine, University of Texas Health Science Center San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA. garling@livemail.uthscsa.edu.
authors: Richard Justin
authors: RJ
authors: Garling
authors: Research Imaging Institute, University of Texas Health Science Center San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA. duongt@uthscsa.edu.
authors: Timothy
authors: T
authors: Duong