Zinc is a mineral found in nearly every cell of our body and is involved in many different chemical reactions. One important role of zinc is in transport for the formation of some proteins.
You may have taken zinc as part of a multivitamin or used it when you have caught a cold. It boosts our immune system and is believed to shorten the length of the illness. And most kids will have had zinc applied to delicate skin to protect from sunburn.
Where do we get our zinc?
The best sources of zinc from our diet is found in seafood such as oysters and crabmeat, red meat, poultry, baked beans, pecans, milk and fortified foods such as breakfast cereals.
What is the role of zinc in the brain?
Scientists have been looking at the role of zinc in our brain. In 2009 a molecular sensor was devised to analyse how much zinc is found in different cells. For example, it was discovered that in the pancreas gland, insulin is packaged around zinc ions. In type two diabetes, this packaging process appears to be defective – this may give further clues as to the molecular changes involved relating to zinc and the development of type two diabetes. As type two diabetes is a risk factor for dementia, being able to reduce the risk at this level would be an important step forward.
Zinc as a regulator of brain cell communication
In the brain, communication between neurons relies on neurotransmitters, special brain chemicals that are packed into vesicles, which also contain zinc. Zinc gets into the brain via special ion channels and glutamate receptors.
It enters the neurons via protein gates called ZIP transporters. Researchers have found that removing these ZIP protein gates in certain areas of the brain such as the hippocampus can protect them from injury.
The hippocampus is the area of the brain where lots of zinc has been found in the neurons. It turns out that having the right amount of zinc at the level of the synapse is essential for normal neuronal communication and function. Too little or too much can lead to neuronal dysfunction or even cell death.
Zinc and Memory
Zinc has been shown to enhance neuronal communication. A team from the Duke University Medical Centre showed that increases in glutamate, the brain’s main excitatory neurotransmitter, enhances this zinc effect and this is thought to be important for memory function. Certain cells in the hippocampus with high levels of zinc were shown to be associated with a particular form of memory formation.
Zinc and Epilepsy
The hippocampus is an area of the brain susceptible to epileptic seizures. In epilepsy those neurons with high levels of zinc are thought to worsen the epilepsy through excessive enhancement of communication. During a seizure these hippocampal cells are then particularly susceptible to damage at a time when they may also be exposed to injury through loss of oxygen and glucose.
Research at the Baylor College of Medicine has shown that if two types of ZIP protein genes were removed, there was less damage to the hippocampal nerves following a seizure. This may help for the future management of epilepsy by leading to the development of drugs targeting removal of the ZIP proteins which will reduce zinc entry into the brain and help to protect the brain’s memory circuits. People who have epilepsy will often remark that their memory is affected in the post ictal or recovery state.
Dr. Jeffrey L. Noebels,Professor of neurology, neuroscience and molecular and human genetics at BCM Director of the Blue Bird Circle Developmental Neurogenetics Laboratory was quoted as saying “These findings pave the way for the development of a new type of neuroprotective medicine for conditions such as seizures, stroke, brain trauma and other neurodegenerative disorders. Many laboratories are looking for such drugs, and this provides an important clue.”
Imperial College London (2009, August 31). Think Zinc: Molecular Sensor Could Reveal Zinc’s Role In Diseases.
Enhui Pan, Xiao-an Zhang, Zhen Huang, Artur Krezel, Min Zhao, Christine E. Tinberg, Stephen J. Lippard, James O. McNamara. Vesicular Zinc Promotes Presynaptic and Inhibits Postsynaptic Long-Term Potentiation of Mossy Fiber-CA3 Synapse. Neuron, 2011; 71 (6): 1116 DOI: 10.1016/j.neuron.2011.07.019
Jing Qian, Kaiping Xu, Jong Yoo, Tim T. Chen, Glen Andrews, and Jeffrey L. Noebels. Knockout of Zn Transporters Zip-1 and Zip-3 Attenuates Seizure-Induced CA1 Neurodegeneration The Journal of Neuroscience, 5 January 2011, 31(1):97-104; doi:10.1523/JNEUROSCI.5162-10.2011