Zinc Homeostasis and Brain Injury

Sensi, Stefano L.; Rockabrand, Erica; Sekler, Israel

doi:10.1007/978-0-387-70830-0_10

Cited by 1 publication

(2 citation statements)

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“…Biochemical studies have shown zinc to be actively involved in the amyloid dysmetabolism associated with Alzheimer's disease (AD) (Bush et al, 1993;Cornett et al, 1998;Cuajungco and Lee, 1997;Danscher et al, 1997;Lovell et al, 1998;Multhaup et al, 1994;Sensi et al, 2007). High concentrations of zinc are observed in the neuritic plaques and cerebrovascular amyloid deposits from both AD patients and ADprone transgenic mice (Corrigan et al, 1993;Friedlich et al, 2004;Lee et al, 1999;Lovell et al, 1998;Suh et al, 2000;Zhang et al, 2008).…”

Section: Alzheimer's Diseasementioning

confidence: 99%

“…Only recently has it been realized that ionic zinc may play a role in the ischemic degenerative events that follow cerebral stroke (Choi, 1996;Galasso and Dyck, 2007;Koh et al, 1996;Sensi et al, 2007;Tønder et al, 1990). In particular, it appears that the hippocampal neurons in the CA1 subregion seem to be selectively affected in this condition (Pulsinelli et al, 1982).…”

Section: Ischemiamentioning

confidence: 99%

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Zinc: The brain's dark horse

Bitanihirwe

Cunningham

2009

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231

154

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Zinc is a life-sustaining trace element, serving structural, catalytic, and regulatory roles in cellular biology. It is required for normal mammalian brain development and physiology, such that deficiency or excess of zinc has been shown to contribute to alterations in behavior, abnormal central nervous system development, and neurological disease. In this light, it is not surprising that zinc ions have now been shown to play a role in the neuromodulation of synaptic transmission as well as in cortical plasticity. Zinc is stored in specific synaptic vesicles by a class of glutamatergic or "gluzinergic" neurons and is released in an activity-dependent manner. Because gluzinergic neurons are found almost exclusively in the cerebral cortex and limbic structures, zinc may be critical for normal cognitive and emotional functioning. Conversely, direct evidence shows that zinc might be a relatively potent neurotoxin. Neuronal injury secondary to in vivo zinc mobilization and release occurs in several neurological disorders such as Alzheimer's disease and amyotrophic lateral sclerosis, in addition to epilepsy and ischemia. Thus, zinc homeostasis is integral to normal central nervous system functioning, and in fact its role may be underappreciated. This article provides an overview of zinc neurobiology and reviews the experimental evidence that implicates zinc signals in the pathophysiology of neuropsychiatric diseases. A greater understanding of zinc's role in the central nervous system may therefore allow for the development of therapeutic approaches where aberrant metal homeostasis is implicated in disease pathogenesis.

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