Exercise: A Key to Preventing Parkinson's Disease
As many as one million Americans suffer from Parkinson’s disease, a degenerative disorder of the central nervous system that affects one’s mobility. Parkinson’s is characterized by the loss of neurons that send messages using the neurotransmitter, dopamine. The condition usually affects people after the age of 60 with symptoms that start as slight tremors, slowly worsening with time to severe rigidity that leaves the individual unable to walk. There is no cure to Parkinson’s, and medication is solely prescribed to alleviate the symptoms and not the root cause of the issue. The abnormal buildup of proteins such as α-Synuclein oligomers in the brain is one of the major causes of death for these neurons and is, therefore, a leading cause of Parkinson’s disease.
Scientists first linked the α-Synuclein gene to Parkinson’s when observing how mutations led to symptoms such as slow motor function, abnormal protein buildup, and general nervous system decline. The α-Synuclein protein in its natural form is highly soluble, spreading through bodily fluids. However, when it becomes mutated as a result of abnormal conditions, these proteins sometimes become insoluble and thus group together to form ‘oligomers’. Recent evidence showed that α-Synuclein oligomers are toxic to the human nervous system, and their presence is important for the development of Parkinson’s. Knowing this, preventing the accumulation of insoluble α-Synuclein oligomers could be the first step towards stopping Parkinson’s disease.
Scientists first linked the α-Synuclein gene to Parkinson’s when observing how mutations led to symptoms such as slow motor function, abnormal protein buildup, and general nervous system decline. The α-Synuclein protein in its natural form is highly soluble, spreading through bodily fluids. However, when it becomes mutated as a result of abnormal conditions, these proteins sometimes become insoluble and thus group together to form ‘oligomers’. Recent evidence showed that α-Synuclein oligomers are toxic to the human nervous system, and their presence is important for the development of Parkinson’s. Knowing this, preventing the accumulation of insoluble α-Synuclein oligomers could be the first step towards stopping Parkinson’s disease.
People suffering from Parkinson’s disease lose neurons at an extremely fast rate.
Image Source: ColiN00B
Because Parkinson’s disease leads to decreasing mobility and increasing body rigidity, physicians often recommend exercise and physical therapy in order to strengthen muscle function. To test the effectiveness of this treatment, scientists placed mice carrying a mutant human version of α-Synuclein in cages with running wheels for 12 months. After three months, they tested the motor and cognitive functions of the mice. After comparing the mutated mice who exercised to those who didn’t, researchers observed that the exercised animals performed much better. As a result, they concluded that exercise improved the function of mice that are expected to suffer from Parkinson’s because of the mutant α-Synuclein they possessed.
Following further tests, researchers found that exercise was associated with greater expression of the PARK7 gene in brain and muscle cells. Mice without PARK7, which encodes the DJ-1 protein, were more likely to have Parkinson’s, leading researchers to believe that DJ-1 proteins guard against developing Parkinson’s by protecting cells from abnormal protein accumulation. Increased PARK7 expression in transgenic mice prevented age-related decline of motor and cognitive abilities normally seen in animals with the transgenic, Parkinson’s-causing gene mutations. Therefore, exercise could improve the abilities of patients expected to have Parkinson’s.
Since an “ounce of prevention is worth a pound of cure,” exercise is essential to keep both the body and mind healthy and free from diseases such as Parkinson’s.
Following further tests, researchers found that exercise was associated with greater expression of the PARK7 gene in brain and muscle cells. Mice without PARK7, which encodes the DJ-1 protein, were more likely to have Parkinson’s, leading researchers to believe that DJ-1 proteins guard against developing Parkinson’s by protecting cells from abnormal protein accumulation. Increased PARK7 expression in transgenic mice prevented age-related decline of motor and cognitive abilities normally seen in animals with the transgenic, Parkinson’s-causing gene mutations. Therefore, exercise could improve the abilities of patients expected to have Parkinson’s.
Since an “ounce of prevention is worth a pound of cure,” exercise is essential to keep both the body and mind healthy and free from diseases such as Parkinson’s.
Featured Image Source: Tumisu
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