The focus of this week’s neurochemistry discussion was Parkinson’s disease. Parkinson’s disease is a progressive neurodegenerative disease that affects movement. Common symptoms of Parkinson’s disease include tremor, bradykinesia (slow movement), stiff limbs, and poor coordination and balance. Like many other neurodegenerative diseases, the cause of Parkinson’s disease is unknown and currently there is no known cure. However, it is known that patients with Parkinson’s disease experience cell death in an area of the brain known as the substantia nigra, which has high levels of a neurotransmitter (chemical signaling molecule) known as dopamine. Dopamine is the neurotransmitter used to regulate and coordinate movement in the body.
Recent research has shown that dysregulation of iron levels in the brain may play a role in the development of Parkinson’s disease (PD) as well as other neurodegenerative disorders. Iron levels have been found to be increased in the substantia nigra in Parkinson’s patients, which has led researchers to believe that regulation of this molecule is linked to PD. Iron is an important molecule in a number of biological processes such as DNA synthesis, cellular transport, storage and activation. A number of proteins are needed to maintain a consistent level of iron in the blood. Iron-regulatory proteins (IRP) and iron-responsive elements (IREs) are in charge of controlling the creation of proteins that regulate the amount of iron allowed in the blood and how much iron is taken into cells. When iron levels increase (not solely due to age) to the point that regulatory proteins are not able to handle the increased concentration, accumulation of iron can have disastrous effects. First, iron reacts with hydrogen peroxide and produces radicals, which cause oxidative stress. Oxidative stress in cells ultimately causes cell death. In other cases, iron causes proteins to accumulate in the cell. One of the hallmarks of Parkinson’s disease is the formation of Lewy bodies, which result from the accumulation of the protein of a-synuclein. Iron accumulation has been shown to contribute to two signs of Parkinson’s disease.
Now knowing that iron accumulation poses a serious threat, what can be done to lower levels of iron? One mechanism of decreasing the adverse effects is through chelation, or binding of iron ions to prevent iron from acting in cells. M30, a synthetic drug that is able to reach the brain, is showing promise in reducing iron levels in the brain and protecting dopaminergic neurons. However, M30 is not the only therapeutic option available for Parkinson’s patients. Surprisingly, there is a simple, natural way that everyone can reduce his or her levels of iron. (-)-epigallocatechin 3-galate (ECCG), an extract of green tea, has been found prevent neuron death in the substania nigra by binding to iron ions. Green tea is readily available and a natural therapy option that may reduce the harmful effects associated with excess iron. Green tea as a therapy option gives patients hope and motivation because they are capable of influencing their risk for Parkinson’s disease through accumulation of iron. Iron dysregulation offers a new, potential target for therapy. Further research is needed to continue looking for a cure for Parkinson’s disease.
You Want Me To Do Drink What…?
