Researchers at the Albert Einstein College of Medicine of Yeshiva University have shed light on the onset of Parkinson's disease, by finding that a glitch in the mechanism through which body's cells recycle damaged components may trigger the degenerative disorder.
The research team believes that the discovery could potentially lead to new strategies for treating Parkinson's and other neurodegenerative diseases.
Earlier studies have shown that mutant forms of a particular protein, known as alpha-synuclein, are poorly digested in the body's recycling scheme, autophagy, of some people with Parkinson's.
In the latest study Dr Ana Maria Cuervo and colleagues studied how several different modified forms of alpha-synuclein influenced autophagy in laboratory tests and in tissue culture.
Results showed that one particular modification of alpha-synuclein interfered with autophagy.
This was the compound created by the interaction of alpha-synuclein with dopamine, the main neurotransmitter produced by the nerve cells damaged in Parkinson's disease.
The researchers argue that the inhibition of autophagy caused by dopamine's alteration of alpha-synuclein could explain the selective death of dopamine-producing nerve cells in Parkinson's disease.
"We propose that inhibition of autophagy caused by dopamine's alteration of alpha-synuclein could explain the selective death of dopamine-producing nerve cells in Parkinson's disease," said Dr. Cuervo.
She also suggested that the interference with autophagy might also have implications in other neurodegenerative diseases including Alzheimer's.
"By devising strategies for boosting autophagy in nerve cells or suppressing the chemical reactions that interfere with the autophagy - by lowering alpha synuclein expression, for example - we may be able to treat patients afflicted with these conditions," said Dr Cuervo.
The study is published in the online issue of The Journal of Clinical Investigation.