11 possible causes of Parkinson´s disease

In most patients, Parkinsons disease may be caused by natural oxidative stress of dopaminergic neurons, hypokinesia and galactose induced oxidative stress. These factors change with age and lifestyle. Lifestyle interventions, including daily exercise and drinking less alcohol and milk, may also delay or prevent Parkinsons disease.

Epidemiological studies of Parkinsons disease have found that there are 11 factors that play an important role in causing or preventing Parkinsons disease. 

It is well known that organochlorine pesticides accumulate in fat deposits in the body, resulting in persistent effects. From the data on paraquat exposure, it can be found that the risk of Parkinsons disease is increased, and the risk ratio is 1.64, which is statistically significant.

α- Synuclein is a protein that may be involved in regulating the release of dopamine and other neurotransmitters, which is very important in Parkinsons disease. B-adrenergic receptor antagonists induce synuclein synthesis genes and increase the risk of Parkinsons disease. B-adrenergic receptor agonists down regulate genes and reduce the risk of Parkinsons disease. 

Chronic alcoholism increased the risk of Parkinsons disease, with a risk ratio of 3.48. Alcohol induced sterol regulatory element binding protein is an obesity factor that leads to visceral fat accumulation. However, obesity has not been shown to be a risk factor for Parkinsons disease. Visceral fat secretes a large number of fat factors harmful to health and brain. One of the adipokines elevated in Parkinsons disease is visfatin, also known as nicotinamide phosphoribosyltransferase. This fat factor destroys the blood-brain barrier by increasing the formation of oxygen free radicals in the brain capillary cavity. The blood-brain barrier is very important for brain health because it regulates the entry of nutrients into the brain and discharges brain waste. The leaking blood-brain barrier may become inflamed, leading to brain inflammation.

Lactose is metabolized in the intestine by lactase and releases glucose and galactose. In bacteria, galactose oxidase metabolizes galactose by producing oxygen free radicals. People with galactosemia show many symptoms of brain oxidative stress, including neurodegeneration, motor imbalance, irregular gait and tremor. These symptoms can also occur in Parkinsons disease. 

Smoking provides nicotine to the brain, a highly addictive substance that interacts with various receptors. Appropriate low doses of nicotine stimulate the release of dopamine in the brain, which is also useful in Parkinsons disease and seems to delay the onset. However, heavy smoking increases the incidence rate of Parkinsons disease, with a hazard ratio of 3.2.

Coffee can prevent Parkinsons disease, with a hazard ratio of 0.52, and contains chlorogenic acid, carverol, caffeinol and other phenols. Coffee has many health effects on Parkinsons disease. 

Tea contains several alkaloids, including theophylline, caffeine and theobromine. Polyphenols in tea have antioxidant activities. Theanine can enhance the activity of dopamine D1 / 5 receptor and may increase the protective effect of alkaloids on Parkinsons disease.

Physical activity can stimulate the production of lactic acid, which is an essential nutrient for brain neurons, endothelium and other cells. Mild oxidative stress induced by exercise induces a protective mechanism beneficial to the brain.

Gout is caused by hyperuricemia, which is more common in obese men. Uric acid is an inflammatory compound that can damage kidneys, joints and other tissues. However, uric acid seems to protect the blood-brain barrier by reducing vascular endothelial growth factor synthesis. The protection of blood-brain barrier is the key to prevent Parkinsons disease.

Vitamin E is a very lipophilic antioxidant, which can protect lipids and other lipophilic molecules from oxidative damage. The protection of blood-brain barrier by vitamin E is of great significance for the prevention of Parkinsons disease. 

The protective effect of ibuprofen may be to reduce the formation of oxygen free radicals by reducing the turnover of dopamine. Cyclooxygenase 2 exists in substantia nigra dopaminergic neurons and is involved in oxygen free radical formation and synaptic plasticity. The activity of this enzyme is increased in Parkinsons disease. This means that ibuprofens inhibition of cyclooxygenase 2 in dopaminergic neurons may have a protective effect on Parkinsons disease.

Summary

Parkinsons disease may be caused by many factors, which lead to the damage of dopaminergic neurons in substantia nigra, and this damage increases with age.

 

 

Cindy