Parkinson's disease can start before birth, suggests study

Parkinson's occurs when brain neurons that make dopamine, a substance that helps coordinate muscle movement, become impaired or die.
Image for representation for Parkinson's Disease.
Image for representation for Parkinson's Disease.

WASHINGTON DC: According to a recent study, people with symptoms of Parkinson's disease before they reach the age of fifty may have brain development disorder even before their birth as the disease can go undetected for 30-40 years before showing the symptoms.

Parkinson's occurs when brain neurons that make dopamine, a substance that helps coordinate muscle movement, become impaired or die.

According to a new Cedars-Sinai research, there is a particular drug that might potentially help correct these disease processes.

Symptoms, which get worse over time, include slowness of movement, rigid muscles, tremors and loss of balance. In most cases, the exact cause of neuron failure is unclear, and there is no known cure

Michele Tagliati, who was a co-author of the study said: "Young-onset Parkinson's is especially heartbreaking because it strikes people at the prime of life. This exciting new research provides hope that one day we may be able to detect and take early action to prevent this disease in at-risk individuals."

To perform the study, the research team generated special stem cells, known as induced pluripotent stem cells (iPSCs), from cells of patients with young-onset Parkinson's disease. This process involves taking adult blood cells "back in time" to a primitive embryonic state.

"Our technique gave us a window back in time to see how well the dopamine neurons might have functioned from the very start of a patient's life," said the study's senior author, Clive Svendsen.

The researchers detected two key abnormalities in the dopamine neurons in the dish. One was the accumulation of a protein called alpha-synuclein, which occurs in most forms of Parkinson's disease

The other abnormality was the malfunctioning lysosomes, cell structures that act as 'trash cans' for the cell to break down and dispose of proteins. This malfunction could cause alpha-synuclein to build-up.

Shlomo Melmed, a dean of the Medical Faculty at Cedars-Sinai said: "This research is an outstanding example of how physicians and investigators from different disciplines join forces to produce translational science with the potential to help patients. This important work is made possible by the dual leadership of Cedars-Sinai as both a distinguished academic institution and an outstanding hospital."

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