Anti-Inflammatory Strategies–Achieving Homeostasis
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Parkinson’s is a disease of the nervous system that affects mobility, memory, and cognition.  Individuals may eventually experience rigid muscles, tremors of the limbs and head, loss of muscle control, monotonous speech levels, and a slow, shuffling gait.

Individuals tend to develop the disease as they age. Having a close relative with Parkinson’s disease (PD) increases the likelihood of developing Parkinson’s, with men more than 1.5 times more likely to develop the disease than females.

Although the causes of Parkinson’s disease are not clear, a recent study suggests that individuals with a specific gene are at a higher risk of getting Parkinson’s disease if they were exposed to pyrethroids, a class of chemicals found in the majority of household insecticides.  Exposure of individuals to these pesticides may result in brain tissue inflammation.

Inflammation and Autoimmune Responses

In Parkinson’s disease, the body mounts an inflammatory response against its own brain cells, its dopaminergic neurons. (An immune response against oneself is called an autoimmune response.)

These specialized brain cells produce a biochemical called dopamine with many functions including controlling bodily movements, memory, ability to think, mood, and learning.  The body’s long-lasting inflammatory response against its own nervous cells gradually destroys the dopaminergic neurons resulting in abnormal dopamine levels and brain activity, symptoms associated with Parkinson’s disease.

Microglial cells are specialized immune cells located in the brain. They are considered the “canary in the mine”.  When microglial cells sense a threat, they become “activated” and release immune factors that may, depending on the types and amounts of these molecules, be beneficial or cause damage to nerve cells.

Activated microglial cells are found in large numbers in the brains of Parkinson’s patients, along with high levels of cytokines, biochemical molecules responsible for inflammation.

The brain and spine of the nervous system are cushioned by cerebrospinal fluid. This fluid helps to provide nutrients to the nervous system and removes waste products from the brain.

Individuals with Parkinson’s disease have high levels of immune inflammatory molecules in their spinal fluid.  The more concentrated the molecules, the more likely the person is to severe fatigue, depression, and cognitive impairment.

Summary

Certain genes that control immune system responses are also strongly linked with the development of Parkinson’s disease.

Increasingly, scientific studies suggest that inflammation and autoimmune responses result in Parkinson’s disease.

Helping the body limit out-of-control inflammation, and achieving a more homeostatic, more balanced immune response, may go a long way towards changing the quality of life in individuals with Parkinson’s.

Feel free to contact Dr. Hellen. There is no fee for speaking with her. Dr. Hellen may be contacted by using this form or at: 302.265.3870 (ET).

 www.nature.com/npjparkd/
www.sciencedirect.com/science/article/pii/S1357272504003711
physrev.physiology.org/content/91/2/461
www.ncbi.nlm.nih.gov/pubmed/25757798
www.ncbi.nlm.nih.gov/pubmed/25769314
www.ncbi.nlm.nih.gov/pubmed/22166438
www.ncbi.nlm.nih.gov/pubmed/25215472
www.ncbi.nlm.nih.gov/pubmed/22814707
www.medicalnewstoday.com/articles/265378.php

An article this week from Shirley Wang, a Wall Street Journal reporter, brought the public’s attention back to the fact that there is no cure for the usually fatal disorder, amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease. Amyotrophic lateral sclerosis (ALS) is a paralytic disease caused by the gradual degeneration of nerve cells in the brain and spinal cord. The breakdown of neruons interrupts the ability of muscles of the body to send messages to the brain. ALS results in difficulties in talking, swallowing, moving, and paralysis, and eventually, the loss of the ability to breathe.

An international group of scientists recently reported in the journal Nature, that the lack of a certain protein might be the common underlying cause of neurodegenerative diseases such as ALS, dementia, Parkinson’s, and Alzheimer’s. The task of this specialized protein is to remove the debris of damaged nerve cells and help in their repair. When this function no longer occurs, normal transmission of signals from muscles to brain is blocked.

One individual commented on Ms Wang’s article. “It seems outrageous to me that in 2011 a quickly fatal disease that was brought to our national attention in 1939 continues to steal our best and brightest without any treatment and with few clues as to the cause. We must do better….”

I agree. Instead of treating a condition after damage has occurred, why not prevent excessive inflammatory responses from causing damage in the first place? The ALS Association does an excellent job explaining that, “The glia cells that usually support and nourish their neighboring neurons in the nervous system can become over active in certain diseases”. And that leads to over production of cytokines, immune signals, that are mediators of inflammation,and damage to the nerve cells.

Inflammation protects the body from infection and repairs tissue damage. But uncontrolled levels of inflammation damages healthy by-stander cells, and tissues. When it comes to the repair protein mentioned above, perhaps individuals with ALS, or other neurodegenerative diseases, are attacking this protein, and decreasing the quantities needed for clean-up and repair.

A body in immune homeostasis, immune balance, is unlikely to attack itself. Instead one approach that research should take is finding ways to help the body modulate inappropriate levels of inflammation.

 

www.ninds.nih.gov/disorders/amyotrophiclateralsclerosis/detail_ALS.htm

www.chicagotribune.com/health/ct-met-northwestern-als-breakthrough-20110822,0,4185292.story

www.nature.com/nature/journal/v477/n7363/full/nature10353.html

http://www.alsa.org/research/about-als-research/inflammation.html

 

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