Parkinson's disease, a movement disorder, has come to be blamed on a combination of genetic and environmental factors.
Parkinson’s disease, a movement disorder that affects at least a half million Americans, has come to be blamed on a combination of genetic and environmental factors.
Although there seems to be some shared risk factors among families, fewer than 10 percent of cases are linked to a single gene mutation, and not every person who carries a gene mutation tied to Parkinson’s develops the condition.
One recent study by researchers at the Parkinson Institute in Sunnyvale, Calif., looked at the histories of 99 pairs of twins, with one twin in each pair suffering from Parkinson’s. The groups were about equally divided between genetically identical twins and fraternal twins.
Among other risk factors, the researchers looked at lifetime work and hobby activities to determine the extent that each subject had been exposed to any of six chemicals linked to Parkinson’s through earlier studies.
Most Read Local Stories
- More wildfire smoke heads into Puget Sound region before rain starts to clear the air
- Wildfire news updates, September 17: What to know today about the destructive fires in Washington state and on the West Coast
- Seattle is in smoke. What's happening to the birds? VIEW
- Coronavirus daily news updates, September 17: What to know today about COVID-19 in the Seattle area, Washington state and the world
- Woman killed in Cal Anderson Park, man found dead after refusing to leave city building, police say
The scientists, led by Drs. Samuel Goldman and Caroline Tanner, found that exposure to two common industrial solvents most raised the risk of developing Parkinson’s: trichloroethylene (TCE), often used as a degreasing agent, and perchloroethylene (PERC), frequently used in dry cleaning.
“The potential importance is great, since both solvents persist in the environment and are commonly used,” Goldman said. “Parkinson’s was sixfold more common in the twins exposed to TCE and ninefold more common in twins exposed to TCE or PERC.”
The study, sponsored partly by the National Institute of Neurological Disorders and Stroke, was published in the Nov. 14 issue of Annals of Neurology.
Parkinson’s is characterized by tremors in the extremities and face, rigidity of the limbs and trunk, slowness of movement and instability or impaired balance and coordination.
Symptoms are usually subtle and gradual, though the disease sometimes progresses rapidly. It usually affects people over age 50, but can occur even in young adults. Although Parkinson’s is considered a chronic, disabling condition, the eventual loss of mobility and inability to speak or even swallow can lead to premature death from infections and other factors.
The disorder is caused by the loss of brain cells that produce dopamine, a signaling chemical that helps regulate movement.
A number of scientists suspect that the culprit in this cell death is the mitochondria, energy-producing organelles inside cells that malfunction and cause neurons in those movement-control areas to die or become impaired.
Researchers at Children’s Hospital Boston studied genetic mutations in a hereditary form of Parkinson’s disease and found that mutations to two proteins leave cells unable to properly dispose of malfunctioning mitochondria.
Unchecked, the mitochondria churn out toxic compounds that damage both nerve cells and contaminate other mitochondria. “It’s the equivalent of an environmental disaster in the cell,” said Thomas Schwarz, senior investigator for the study published in the Nov. 11 issue of Cell.
Schwarz and his colleagues are looking at possible gene therapies that would either restore neurons’ ability to flush out faulty mitochondria or ramp up production of healthy structures in sufficient numbers to overcome the damage. “We may need to do both,” he said.
Similar damage to mitochondria has also been noted in other neurodegenerative diseases, including Alzheimer’s, Huntingdon’s and Lou Gehrig’s disease (amyotrophic lateral sclerosis).
Other researchers at the National Heart, Lung and Blood Institute reported in August, in the Journal of Clinical Investigation, that one of the suspect proteins, called Parkin, is involved in transporting and regulating the types and amount of fat found in many organs throughout the body.
The researchers found that mice with defective Parkin could not gain weight, and that cells from people with Parkin mutations had less ability to absorb fat.
Dr. Michael Sack, the study leader, noted that the cells in the substantia nigra are among the most active in the brain, each with more than 300,000 connections and constantly transmitting information. If the cells’ fat and cholesterol membranes are not properly arranged, they could be more susceptible to damage and poor performance, he said.
(Contact Lee Bowman at email@example.com.)