Ischemic Brain Injury in Hyperhomocysteinemia Book Title: Cerebral Ischemia; ISBN: 978-0-6450017-9-2

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Jan Lehotsky, PHD, DSC
Maria Kovalska, PHD
Eva Baranovicova, PHD
Petra Hnilicova, PHD
Dagmar Kalenska, PHD
Peter Kaplan, PHD

ABSTRACT


Homocysteine is an intermediate product of methionine metabolism. Hyperhomocysteinemia can be caused by high intake of methionine, deficiency of vitamin B12, folate, or both. Hyperhomocysteinemia causes cardio- and cerebrovascular diseases, including ischemic stroke. Hyperhomocysteinemia-induced oxidative stress, inflammation, and endoplasmic reticulum stress play an important role in the pathogenesis of several neurodegenerative diseases. Pyramidal neurons of the hippocampus are sensitive to prolonged levels of homocysteine due to the absence of metabolization by transsulfuration as well as by folate- or B12- dependent remethylation. This chapter highlights the role of hyperhomocysteinemia in neurodegenerative changes following cerebral ischemia. An overview of how hyperhomocysteinemia by itself, or in combination with ischemia-reperfusion injury, exacerbates neurodegeneration is presented. The role of hyperhomocysteinemia in amyloid deposition and hyperphosphorylation of tau protein in the brain, along with plasma metabolic alterations in cerebral ischemia-reperfusion injury is reviewed. Prevention of hyperhomocysteinemia may have therapeutic implications in cerebral ischemic stroke and deserves investigation.  

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