Short Communication Open Access
Volume 1 | Issue 4 | DOI: https://doi.org/10.33696/Neurol.1.022

The Odyssey of Alpha-synuclein and Neuroinflammatory Mediators as Potential Candidates in the Aetiology of Parkinsons Disease

  • 1Department of Medical Physiology, University of Nairobi, Nairobi, Kenya
  • 2University Hospital Wuerzburg, Clinic and Policlinic for Psychiatry, Psychosomatics and Psychotherapy Margarete-Hoeppel-Platz 1, 97080, Wuerzburg, Germany
  • 3University of Southern Denmark Odense, J.B. Winslows Vey 18, 5000, Odense, Denmark
+ Affiliations - Affiliations

Corresponding Author

Jeswinder Sian-Hulsmann, j.sian@germanmedicalcenter.net

Received Date: July 04, 2020

Accepted Date: August 25, 2020


There is a myriad of potential candidates suggested to be associated to the aetiology of Parkinson’s disease, of these a-synuclein appears to the first runner up. This notion is endorsed by the appearance of a-synuclein aggregates (present in Lewy bodies) in close proximity to regions exhibiting neuronal cell loss. The mechanism(s) contributing to its accumulation include, some genetic dysfunction, overproduction of the protein, misfolding, inability to effectively degrade the misfolded form. Furthermore, the ability of a-synuclein to operate as ferrireductase, allows it to produce reactive oxygen species and exacerbate the oxidative stress related cytotoxic processes in the illness. The accumulation of misfolded a-synuclein may also invoke the release of inflammatory mediators. The presence of microgliosis in the substantia nigra in the disease reflects the occurrence of inflammation. The destructive role of neuro-inflammation in degenerative diseases is exhibited by the neurological manifestations produced by infectious agents such as bacteria and viruses. Therefore, these findings offer many budding therapeutic interventions that can be advocated in the disorder. However, an urgent need for a biomarker is warranted to detect the disease early in order to halt or delay its progression.



Alpha-synuclein, Microglia, Neuroinflammation, Substantia nigra, Neuronal death, Parkinson’s disease

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