Brain ischemic

Fukunaga, K., and Kawano, T. (2003). Akt is a molecular target for signal transduction therapy in brain ischemic insult. J. Pharmacol. Sci. 92, 317-327. 

G. Calapai, M. C. Marciano, F. Corica, A. Allegra, A. Parisi, N. Frisina, A. P. Caputi, M. Buemi, Erythropoietin protects against brain ischemic injury by inhibition of nitric oxide formation, Eur J Pharmacol 401, 349-56(2000). 

Stroke. A stroke is an interruption of the blood supply to any part of the brain. Stroke can be caused by either a clot obstructing the flow of blood to the brain (ischemic) or by a blood vessel rupturing and preventing blood flow to the brain (hemorrhagic). Ischemic stroke comprises the majority of all strokes (approximately 85%). 

Al-Jamal,K.T.,Gherardini, L., Bardi,G., Nunes, A., Guo, C.,Bussy,C.,Herrero,M.A., Bianco, A., Prato, M., Kostarelos, K., Pizzorusso, T., 2011. Functional motor recovery from brain ischemic insult by carbon nanotube-mediated siRNA silencing. Proc. Natl. Acad. Sci. U. S. A. 108, 10952-10957. 

Traumatic brain injury is the most common cause of death in subjects under the age of 40, and an important risk factor for AD. Loss of hippocampal cells and depletion of ACh and of muscarinic receptors can be attenuated in injured experimental animals, improve blood perfusion in ischemic areas and increase cholinergic transmission in cortex and hippocampus the same mechanism invoked for treatment of VD. 

Findings obtained from experimental studies suggest that induction of iNOS mediates inflammatory or ischemic brain damage and that excessively activated nNOS under excitotoxic or ischemic conditions produces NO that is toxic to surrounding neurons. Selective inhibition of iNOS or nNOS may be neuroprotec-tive. This is also the case in glaucoma and diabetic... 

Reduction of the risk of transient ischemic attacks or strokes in men who have had transient ischemia of the brain due to fibrin platelet emboli (aspirin only). This use has been found to be effective only in men (not women). 

Miller RJ, Banisadr G, Bhattacharyya BJ (2008) CXCR4 signaUng in the regulation of stem ceU migration and development. J Neuroimmunol 198 31-38 Minami M, Satoh M (2003) Chemokines and their receptors in the brain pathophysiological roles in ischemic brain injury. Life Sci 74 321-327... 

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. 

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