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Is zinc the link between compromises of brain perfusion (excitotoxicity) and Alzheimer's disease?

作者信息

Frederickson Christopher J, Cuajungco Math P, Frederickson Cathleen J

机构信息

NeuroBioTex, Inc. & The University of Texas Medical School, Galveston TX 77550, USA.

出版信息

J Alzheimers Dis. 2005 Nov;8(2):155-60; discussion 209-15. doi: 10.3233/jad-2005-8208.

DOI:10.3233/jad-2005-8208
PMID:16308484
Abstract

Prior brain injury is a major risk factor in the development of Alzheimer's disease. This is true for traumatic brain injury, stroke or ischemic brain injury, and (more speculatively) for brain injury resulting from the hypo-perfusion-reperfusion in cardiac arrest or cardiac bypass surgery and even hypo- or hypertension. Here we propose that the release of excess, toxic, "floods" of free zinc into the brain that occurs during and after all excitotoxic brain injury is a key factor that sets the stage for the later development of Alzheimer's disease. Rapid and aggressive administration of zinc buffering compounds to patients suffering brain injury may therefore not only ameliorate the acute injury but might also reduce the risk of subsequent development of Alzheimer's disease.

摘要

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