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

Issue title: Dedicated to Prof. Marino Nicolini

Article type: Research Article

Authors: Frederickson, Christopher J.^a | Cuajungco, Math P.^b | Frederickson, Cathleen J.^{a; *}

Affiliations: [a] NeuroBioTex, Inc. & The University of Texas Medical School, Galveston TX 77550, USA | [b] Harvard Medical School, Department of Otology and Laryngologist, and Massachusetts Eye and Ear Infirmary, Eaton-Peabody Lab, 243 Charles Street, Boston MA 02114, USA

Correspondence: [*] Corresponding author. E-mail: cathy@neurobiotex.com.

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.

DOI: 10.3233/JAD-2005-8208

Journal: Journal of Alzheimer's Disease, vol. 8, no. 2, pp. 155-160, 2005