Iron imbalance associated with Parkinsons disease

October 14, 2004 Printer Friendly
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Iron imbalance associated with Parkinson’s disease


Parkinson’s disease

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Iron imbalance associated with Parkinson’s disease
Although having either too little or too much iron can contribute to the development of Parkinson’s disease, having too much iron is far worse, according to Florida State University researcher Cathy Levenson. Dr Levinson is the author of a report entitled, "The Role of Dietary Iron Restrictions in a Mouse Model of Parkinson's Disease,” which will appear in a future issue of the journal Experimental Neurology.

Dr Levenson, who is an associate professor of nutrition, food and exercise sciences at FSU's College of Human Sciences, stated, "We define our work here at the cellular level. Our primary research objective is to better understand how trace metal imbalances, which are associated with neuropsychiatric and neurodegenerative diseases, affect the molecular mechanisms that regulate gene expression."

Dr Levenson and colleague Mark Mattson of the National Institute on Aging fed healthy mice and mice at risk of Parkinson’s disease varying amounts of iron. They found that high levels of iron were associated with the onset of Parkinson’s-like symptoms such as tremors in healthy mice, and appeared to accelerate the disease in mice that had already developed it. Low levels of the mineral delayed the onset of symptoms and slowed the disease’s progress.

In healthy mice, reduced iron levels also decreased the neurotransmitter dopamine, whose diminishment in Parkinson’s disease is responsible for the disease’s symptoms. Nevertheless, elevated iron levels remain more dangerous than low levels in their ability to increase the onset and progression of Parkinson’s disease.

This study shows that both low and high levels of iron are associated with the genes and neuron suicide that lead to reduced dopamine production and Parkinson’s disease.


Parkinson’s disease
Parkinson's disease (also called paralysis agitans) is a degenerative central nervous system disorder. Parkinson's disease is generally a disease of unknown cause, affecting persons over the age of 60 (Glanze 1996). In the United States, about 1% of individuals (1 in 200) over the age of 60 are affected (Clayman 1989). However, the disease may occur in younger persons, particularly following inflammation of the brain (encephalitis) or from poisoning by carbon monoxide, metals, or certain drugs.

Iron overload can intensify Parkinson's disease. Not only do Parkinson's patients have low levels of natural antioxidants, such as glutathione and superoxide dismutase, but they may also have high levels of iron in the substantia nigra area of the brain (Youdim et al. 1991; Good et al. 1992; Olanow 1993). Iron tends to catalyze free-radical reactions that destroy dopamine-producing cells (Linert et al. 2000). Potential sources of iron are from inadvertent or accidental ingestion of iron supplements, drinking water, iron plumbing pipes, and cookware. In addition to the brain, target organs are the liver, cardiovascular system, and kidneys (Roberts 1999).

The symptoms of Parkinson's disease are attributed to a loss of brain cells in the basal ganglia (Clayman 1989). These cells produce the neurotransmitter dopamine. There also seem to be abnormalities in other parts of the brain and in the availability of other neurotransmitters, such as serotonin and norepinephrine (Adam et al. 1983; Kish et al. 1984; Stern et al. 1984; Taylor et al. 1986; Ring et al. 1994; Arahata 1999; Bohnen et al. 1999; Narabayashi 1999).

Supplementation with nutrients has reported benefits for persons with Parkinson's disease. These supplements include amino acids, antioxidants, coenzyme Q10, melatonin, folic acid, acetyl-L-carnitine, octacosanol, phosphatidylserine, NADH, and the European drug Hydergine (Snider 1984; Yapa 1992; Mizuta et al. 1993; Schulz et al. 1995; 1996; Shults et al. 1997; 1998; 1999; Beal et al. 1998; Golbe et al. 1998; Sakagami et al. 1998; Seitz et al. 1998; Beal 1999; Jimenez-Jimenez et al. 2000; Kidd 2000; Nadlinger et al. 2001; Roghani et al 2001; Ross 2001; Tan et al. 2001; Zisapel 2001; Antolin et al. 2002; Chen et al. 2002; Duan et al. 2002).

Drugs such as L-dopa alleviate symptoms of Parkinson's disease but are not believed to slow the underlying disease process. A recent study found evidence that CoQ10 may help stop the specific brain cell death that causes Parkinson's (Shults et al. 2002).

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The brain also needs a tremendous amount of energy to function properly. And, since coQ10 is one of the most efficient mitochondrial energy enhancers, it is logical to expect that this energy-enhancing nutrient could play a role in brain function.

It is a fact that coQ10 diminishes with age. This means mitochondrial energy decreases accordingly, leading to what is now being referred to as "mitochondrial disorders" or simply put, suboptimal health, as cellular energy and function are compromised.

L-tyrosine tablets

L-tyrosine can be converted by neurons in the brain to dopamine and norepinephrine (noradrenaline), hormones, which are depleted by stress, overwork and certain drugs. By replenishing norepinephrine in the brain, mental energy levels are enhanced and a feeling of contentment often occurs. Because of the liver conversion necessary for L-phenylalanine to have these effects, L-tyrosine is often faster acting. In addition, the conversion step from L-tyrosine to norepinephrine may be enhanced if the cofactors (vitamins B6 and C) are included.

Questions? Comments? Send them to or call 954 766 8433 extension 7716.

For longer life,

Dayna Dye
Editor, Life Extension Update
1100 West Commercial Boulevard
Fort Lauderdale FL 33309
954 766 8433 extension 7716

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