Iron is an essential mineral that plays an important role in various physiological processes.

However, excessive accumulation of iron in certain tissues can be harmful and has been associated with several diseases, including Parkinson’s disease (PD).

What is Parkinson’s disease?

PD is a neurodegenerative disorder characterized by the gradual loss of dopaminergic neurons in a part of the brain called the substantia nigra. Dopamine is a neurotransmitter that plays an important role in controlling movement, mood, and reward.

As the number of dopamine-producing neurons decreases, the symptoms of PD start to appear, including tremors, rigidity, and difficulty moving.

The link between iron accumulation and Parkinson’s disease

Studies have shown that iron accumulation in specific regions of the brain is associated with an increased risk of PD. Iron is essential for many biological processes, including cellular respiration and DNA synthesis.

However, excess iron can promote oxidative stress and damage DNA and other cellular components, leading to cell death and tissue damage. In addition, iron accumulates in the form of iron deposits called ferritin in the brain regions responsible for motor control, including the basal ganglia, globus pallidus, and substantia nigra.

Ferritin is a storage protein that binds iron, preventing its toxicity by sequestering it into an inert complex. However, ferritin itself can become toxic when it accumulates in high amounts and induces inflammation and cell death.

In PD patients, ferritin levels are elevated in the brain regions affected by the disease, indicating that iron accumulation and ferritin formation may be a contributing factor to dopaminergic neuron loss and motor dysfunction.

Iron dysregulation in PD patients

Iron dysregulation is a hallmark of PD pathology, as it has been observed that total iron concentrations increase in different brain regions in PD patients compared to control subjects.

The changes in iron distribution in PD brains also lead to high levels of oxidative stress and cell death, and ferritin levels are higher in the substantia nigra of PD patients.

Iron dyshomeostasis occurs in the very early stages of the disease and may play a role in the pathogenesis of PD.

However, it is not yet clear whether the increased iron concentration is the result of the disease process or contributes to it, as high levels of iron accelerate oxidative stress, which can cause damage to cells.

Consequences of iron accumulation

Iron accumulation can have a variety of negative consequences on health and well-being.

It can lead to cellular damage, inflammation, and oxidative stress, all of which have been implicated in the pathogenesis of various neurological conditions, including PD. Iron accumulation has also been linked to the damage of cellular DNA, leading to mutations and cancer risk.

In addition, high levels of iron in the brain can exacerbate the effects of other environmental toxins, such as pesticides, that are known to increase the risk of PD.

There is also evidence that iron accumulation in the brain can damage the blood-brain barrier and promote inflammation, which can further contribute to motor dysfunction.

Treatment options

The link between iron accumulation and PD has led to interest in using iron chelation therapy, which can reduce iron levels in the body. Iron chelators are molecules that bind to iron and facilitate its excretion from the body.

Several iron chelators have shown promise in clinical trials and have been evaluated in PD patients, although the results have been mixed. While iron chelation therapy may be beneficial in preventing or slowing the progression of PD, more research is needed to better understand its safety and efficacy in PD patients.

Other potential therapeutic strategies for PD targeting iron dysregulation include the use of dietary supplements, such as antioxidants and vitamins, and lifestyle changes that can reduce oxidative stress and inflammation, such as exercise and stress management techniques.

Conclusion

Iron accumulation in certain parts of the brain is associated with an increased risk of PD, likely due to the role of iron in promoting oxidative stress and inflammation.

Iron dysregulation is an early event in the pathogenesis of PD, and could be a therapeutic target for prevention or slowing down of disease progression. Iron chelation therapy is one potential strategy to reduce iron levels in the body and brain, but more research is needed to fully evaluate its safety and efficacy in PD patients.