In Parkinson’s disease (PD) there is slow and progressive loss and deterioration of nerve cells of the brain especially those involved with regulation and control of movements.

In a healthy person, an adequate amount of dopamine (a chemical messenger present in the body) is present in substantia nigra (an area of cluster of nerve cells in the brain). Normally, dopamine is carried by the nerve cells from this area to another cluster of nerve cells known as the corpus striatum where these nerves terminate. Here, along with dopamine, acetylcholine, another chemical messenger, regulates the bodily movements.

In a patient with Parkinson’s disease there is an imbalance between these two chemical messengers. In most of the cases, there is loss of dopamine in the substantia nigra and degeneration of dopamine nerve terminals in the corpus striatum.

Approximately 60-80% of dopaminergic neurons are lost before the motor signs of Parkinson disease emerge. Rarely, the hyperactivity of acetylcholine nerve cells may be the underlying cause of Parkinson’s disease. Another change observed in some cases is the presence of protein clusters known as “Lewy bodies” in the brain, which are characteristic, but not specific of PD.

At present, it is believed that PD is mainly caused by environmental factors and hereditary factors. A genetic predisposition (i.e. higher risk of disease if any close relative is suffering from PD) has been seen in the patients. There are very rare families where PD is inherited.

Oxidative Stress in Parkinson’s Disease

The possible role of environmental risk factors associated with the development of disease include use of pesticides, consumption of contaminated well water, exposure to herbicides, and proximity to industrial plants or quarries. The most accepted theory establishing the link between these factors and degeneration in the brain is that of “oxidative stress”.

The role of oxidative stress (increased levels of free radicals) in PD has been extensively studied. The utilization of energy in the brain can lead to increase in the concentration of free radicals (unstable highly reactive chemical compounds) e.g. hydrogen peroxide. In healthy individuals a balance is maintained between antioxidants and oxidative ions and thus oxidative stress does not occur. But in patients of PD, increased concentrations of free radicals and decreased levels of antioxidants have been observed which lead to nerve damage by lipid per-oxidation and pore formation in the cell membranes.

Drugs that Affect the Brain Chemistry in PD

The presently available treatments are symptomatic i.e. they treat the disease but do not alter the underlying degenerative process. These are helpful in restoring and maintaining function and quality of life for many years. Most of the drugs help in restoring dopamine levels in the brain. They either :

• increase the synthesis of dopamine (e.g. levodopa and carbidopa combination)
• enhance the action of dopamine (e.g. ropinirole, pramipexole)
• decrease the degradation of dopamine (e.g. selegiline – selective inhibitor of MAO-B / Mono amine Oxidase B, an enzyme degrading dopamine)
• inhibitors (tolcapone and entacapone) of another degrading enzyme, COMT / catechol-O-methyl transferase

The symptoms of PD in patients taking certain drugs especially antipsychotics like chlorpromazine can be treated by giving anticholinergic drugs like benztropine. The drugs which increase the dopamine levels are not helpful in these patients. The preventive role of antioxidants is still under study.

The biggest single risk factor associated with contracting Parkinson’s disease is old age; men also stand a higher chance of it than do women. Family history is also another factor particularly when a first generation family member has the disease, if this family member is a parent or sibling then chances are estimated to double for yourself to developing the disease. It is thought that this increased risk is due to a number of factors including genetic and environmental which close relations have in common.

The one single factor which has been most consistently associated with a reduced risk of Parkinson’s disease is smoking, the exact reasons for this has never been determined but smoking does seem to offer some protection against developing Parkinson’s disease. However the negative effects that smoking has on our health far outweighs the benefit of not developing Parkinson’s from smoking, it should by no means be considered as a way of preventing the disease.

Environmental causes of Parkinson’s disease

Most cases of Parkinson’s disease are thought to come about as a result of environmental factors and possible interactions of genes. Environmental factors such as the build up of weak toxins may eventually lead to Parkinson’s in those people who are genetically predisposed. The actual identity of these toxins is unknown but several risk factors due to the environment have been identified through epidemiological studies.

One factor that is persistent however is the finding that rural living, exposure to drinking water from wells and agricultural work increases the risk of developing Parkinson’s disease. This could suggest that pesticides and herbicides might play a crucial role or at the very least contribute to the development of the disease.

However it should be remembered all these factors by no means will determine that you will develop Parkinson’s disease because many people who are constantly confronted with these factors never do develop the illness.

The role genetics play

While there are several genes that are thought to contribute to Parkinson’s disease it should be noted that they are a factor which only accounts for a very small amount of the cases diagnosed. One of the most noted genes is called the parkin; this gene creates a protein which it was named after, parkin.

Its role is to help breakdown defective proteins inside the brain cells, when the gene is altered this leads to function impairment. For a person to develop Parkinson’s disease two altered copies of parkin are needed.

This type of inheritance is called autosomal recessive and requires that one copy of the recessive gene is inherited from each parent. Developing Parkinson’s disease this way usually occurs with people in their 40`s, with parkin being the most common of genetic causes of Parkinson’s disease.

Millions of people throughout the world suffer every year from chronic allergies; these can be allergies from their pets, to dust and spores. A recent study has shown that these people who suffer from chronic allergies are up to three times more likely to develop Parkinson’s disease at some time in their life.

Sufferers of allergic rhinitis which is an allergy in which the sufferer seems to have a permanent cold appear to be at much greater risk of developing Parkinson’s. The research conducted gathered information which showed a link to conditions which cause inflammation and breakdown of brain cells and found a decidedly big increase in cell death in people suffering from rhinitis.

This research is indeed worrying as there are thought to be over five million people in the UK alone who suffer from perennial allergic rhinitis, a condition which more often than not is triggered by allergens such as the house dust mite, skin flakes from pets and spores.

Researchers are now speculating that the inflammation which is caused by the allergy may release certain chemicals into the brain which inadvertently kill brain cells, which is exactly what happens in Parkinson’s disease. Scientists however did stress however that the study didn’t prove that allergies were a cause of Parkinson’s disease but rather that there was an association between the two.

The study primarily came about from another study which showed that people who took anti inflammatory drugs on a regular basis were less likely to develop Parkinson’s disease. The concluding results of this test then prompted scientists to look deeper into the link between Parkinson’s and diseases which are characterised by inflammation.

The study was made looking at 196 people who had developed Parkinson’s disease and matched them with people of a similar age and sex who didn’t have Parkinson’s, they were then studied over a period of 20 years.

Both of the groups were then examined to find out if the people suffering from Parkinson have had more inflammatory diseases, from this study scientists concluded that those who had allergic rhinitis were 2.9 times more likely to go on to develop Parkinson’s disease.

Therefore the association with getting Parkinson’s disease is increased to almost three times as much as that of someone who doesn’t suffer from allergic rhinitis, which scientists said was a very high elevation.

It is thought that people who have allergic rhinitis mount an immune response with their allergy so that they become more likely to mount that same response in the brain as well, which then would lead to inflammation. The brain then responds by releasing certain chemicals which then inadvertently kill cells in the brain the same as is seen in Parkinson’s disease.