The Implications of α-synuclein in the Treatment of Parkinson’s Disease

Kelly M. Wilmas,
University of Texas at Austin

Full paper: www.kon.org/urc/v12/wilmas.html

Abstract This purpose of this research is to provide valuable information regarding the pathways that cause aggregation of the α-synuclein protein in brain nerve terminals, causing neurodegeneration and motor dysfunction, in order to diagnose Parkinson’s disease early and provide effective treatment. Studies have shown that the idiopathic form of Parkinson’s is strongly associated with changes in α-syn expression due to mutations and single nucleotide polymorphisms, which causes aggregation of α-syn protein into amyloid deposits in brain nerve terminals. Familial Parkinson’s disease is due to autosomal-dominant inheritance of the mutated α-syn. Thus, α-syn is thought to play a fundamental role in the genetic etiology of Parkinson’s and can possibly be targeted in order to treat the disease. In order to gather more evidence of this, I compiled primary and review research articles on the genetic mechanisms of this protein. In this review, I provide an overview of known interactions of the protein with the environment, genes, and aging process. I also include significant findings that improve our understanding of possible treatment options, targeting α-synuclein, for this debilitating disease.

Introduction Parkinson’s disease is currently the second most prevalent neurodegenerative disease in existence, affecting 6.3 million people worldwide (Baker, 2004). Presently, there is no cure for the disease, and it causes substantial morbidity. The main pathology of Parkinson’s disease is degeneration of the dopaminergic substantia nigra pars compacta of the brain (McNaught & Jenner, 2001). It supplies the striatum, which is involved in modulating movement pathways and executive functions, with dopamine when functioning normally. However, neurodegeneration prevents this from occurring (McNaught & Jenner, 2001). The neurotransmitter dopamine relays messages to the brain in order to control movement and cognitive function, but the nerve cells that produce dopamine are at least 70 percent lost when Parkinson’s symptoms develop (Heisters, 2011). Due to degeneration of these neurons associated with dopamine in the brain, affected individuals experience motor symptoms that include slow or rigid movement, tremors while at rest, or impaired posture and balance. Patients devastatingly lose the control over their own bodies, mentally and physically. Parkinson’s does not discriminate against any nationality, gender, age, or race; many people will know someone with Parkinson’s in his or her lifetime and witness that person’s struggle. The disease is progressive in that the symptoms will continue to worsen until death results, although its rate of progression differs among individuals (Worth, 2013). The exact cause of neurodegeneration in the substantia nigra remains unknown, but through continuous experimentation and inquiry, it is possible to find the cause and apply new treatments.

Read the full paper: www.kon.org/urc/v12/wilmas.html