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Recent scientific advances have allowed researchers to better define the mechanisms of action (MOA) underlying Parkinson’s disease (PD). Such developments in PD research serve to expand the fundamental knowledge of the disease, referred to as the “shaking palsy” back in 1817. The article explores some of the steps necessary to further optimize PD therapy and treatment as well as its relationship to asthma. getAbstract recommends this article to physicians and scientists concerned with the treatment of PD.

In this summary, you will learn

  • What the cause of Parkinson’s disease (PD) is,
  • What asthma and Parkinson’s disease have in common, and
  • How β2-adrenoreceptor agonists directly influence PD pathogenesis. 
 

About the Author

Evan Snyder is director of the Center for Stem Cells and Regenerative Medicine at Sanford Burnham Prebys Medical Discovery Institute in California. Snyder obtained his MD and PhD in neuroscience from the University of Pennsylvania.

 

Summary

Scientists know what causes Parkinson’s disease (PD) and research is shifting towards medication that targets its source.

Parkinson’s disease (PD) is defined by the deficiency of dopamine in the brain. One of the major hubs for brain cells that release the neurotransmitter dopamine (DA) – the substantia nigra (SN) – is located in the brainstem. Since 1960, PD therapy has concentrated on the replenishment of dopamine in the brain. When a patient is resistant to treatment, the source of the problem is difficult to determine. In addition, DA provision is not the best therapy, as it fails to obstruct PD pathogenesis. An effective PD treatment should target the cause of DA depletion. The dopaminergic neurons become dysfunctional after protein folding goes awry and protein aggregates called Lewy bodies (LB) form. With that in mind, further research was conducted to determine the genetic and intracellular influences on LB formation. LBs are composed of α-synuclein (α-syn) and their presence is correlated with the severity of PD. The gene responsible for the expression of α-syn is SNCA. The transcription of SNCA directly affects the amount of α-syn inside of a cell. Given a cell’s failure to breakdown pathological α-syn, PD may be considered a “synucleinopathy.” 


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