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Zinc in traumatic brain injury: from neuroprotection to neurotoxicity

Morris, Deborah R.a; Levenson, Cathy W.a,b

Current Opinion in Clinical Nutrition & Metabolic Care: November 2013 - Volume 16 - Issue 6 - p 708–711
doi: 10.1097/MCO.0b013e328364f39c
MICRONUTRIENTS: Edited by Gil Hardy and Henry C. Lukaski

Purpose of review In light of the recent recognition that even mild forms of traumatic brain injury (TBI) can lead to long-term cognitive and behavioral deficits, this review examines recent data on the neuroprotective and neurotoxic roles of zinc after brain injury.

Recent findings Data show that treatment using dietary and parenteral zinc supplementation can reduce TBI-associated depression and improve cognitive function, specifically spatial learning and memory. However, excessive release of free zinc, particularly in the hippocampus associated with acute injury, can lead to increases in protein ubiquitination and neuronal death.

Summary This work shows the need for future research to clarify the potentially contradictory roles of zinc in the hippocampus and define the clinical use of zinc as a treatment following brain injury in humans. This is particularly important given the finding that zinc may reduce TBI-associated depression, a common and difficult outcome to treat in all forms of TBI.

aDepartment of Biomedical Sciences

bProgram in Neuroscience, Florida State University College of Medicine, Tallahassee, Florida, USA

Correspondence to Cathy W. Levenson, PhD, Florida State University, College of Medicine, Tallahassee, FL 32306-4300, USA. Tel: +1 850 644 4122; fax: +1 850 644 5781; e-mail:

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins