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Skip Navigation LinksHome > Programs and Activities > ODS Seminars, Conferences, and Workshops > Zinc Conference > Zinc Workshop Abstract > Zinc Summary > Session V, Zinc and the Central Nervous System

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Session V, Zinc and the Central Nervous System

Zinc and Health: Workshop Summary

Session V

Session V, Zinc and the Central Nervous System focused on the anatomy, physiology,  functional implications, and the pathology of zinc in the CNS. The fact that zinc is present in two distinctly different "pools" in the brain was recognized as an important starting point for discussion. The major pool, which is protein-bound, was recognized as an essential component of  literally dozens of zinc metalloenzymes and other zinc metalloproteins. These zinc metalloproteins are ubiquitous in all soft tissue and in essentially all organelles of all cells. 

The other pool  (synaptic zinc) was described as small in quantity (less that 5% of the total zinc) but large in functional significance.  The synaptic zinc was described as   the small pool that is stored exclusively in the presynaptic vesicles of certain forebrain neurons, and released in a calcium- and impulse dependent fashion, resulting in transitory "surges" of free or weakly-bound Zn2+ ion appearing in the brain's extracellular fluid. These zinc-containing neurons were shown to be almost exclusively located in cerebrocortical (especially allocortical) and amygdalar circuit, releasing their Zn2+ signals primarily in those brain regions. The impact of Zn2+ signals upon post-synaptic receptors (especially amino acid receptors) and the neurotoxic effects of excess synaptically- released Zn2+  (as occurs in seizures, ischemia, and head trauma) were both reviewed. 

The turnover and life-cycle of  presynaptic vesicular zinc was also a focus of interest.  After synaptic release into the cleft, zinc ions are taken up into the boutons by a high-affinity, energy-dependent transport process associated with the boutons. This uptake can replenish the vesicles, possibly working in concert with the ZnT-3 protein found exclusively in the presynaptic vesicles of zinc-containing synaptic boutons.

The role of zinc in cognitive function has been studied extensively in both children and the elderly.  It was noted that zinc deficiency during fetal life is associated with developmental delays; that zinc repletion in children with zinc deficient gestations may not be adequate to improve all of the developmental consequences.  Low serum zinc levels in elders are associated with poorer global cognitive function, particularly verbal function, and that there is an inverse correlation of zinc blood levels with plaque density in Alzheimer's disease. Lower serum zinc levels are associated with slower lower extremity function and poorer activities of daily living. Repletion in elders with lower serum zinc levels is associated with improved, but variable cognitive function, and especially with activities of daily living.  It was noted that zinc's most important cognitive effects may be mediated in conjunction with other micronutrients. 

Zinc deficiency is likely an exacerbating or accelerating factor associated with the syndrome of  anorexia nervosa. Studying the changes in appetite regulation, such as the "leptin-NPY-appetite axis" during zinc deficiency may prove to be a useful model for physiologic changes occurring during anorexia nervosa.  The impact of zinc deficiency upon food intake may also be mediated in part by the paleophobia triggered by malnutrition.

Evidence was presented showing an intimate association of zinc and Alzheimer's disease in the terms of the pathogenesis of Alzheimer's.  Zinc may play a role in the elaboration of the apoptotic pathways that are governed by zinc concentrations within the brain, and may also impact on the generation of neurofibrillary tangle formation and the basic biology of tubulin assembly. Alzheimer's disease is characterized by amyloid deposits within the neocortical parenchyma and within the cerebrovascular area of the brain. Evidence was presented showing that  these amyloid deposits are selectively enriched in zinc and showing that  zinc chelation may dissolve amyloid lesions. The possible use of zinc chelators as a therapeutic approach to treat neuro-toxicities derived from any amyloid deposits has been considered.