Florida Atlantic University (FAU) neuroscientist and collaborators link inflammation, olfaction and pathology seen in Parkinson’s disease (PD). Their research appears in Brain Pathology.

Since mounting evidence indicates that neuroinflammation contributes to the development and progression of PD and other degenerative diseases, scientists have proposed that the initial impact of environmental toxins inhaled through the nose may induce inflammation in the brain, triggering the production of Lewy bodies that can then be spread to other brain regions. However, the relationship linking olfactory dysfunction and PD development remains unclear.

[RELATED: Does the Nose Know Parkinson’s? ]

Ning Quan, PhD, a neuroscientist from FAU’s Schmidt College of Medicine and a faculty member of the FAU Brain Institute (I-BRAIN), is among a team of researchers with new findings that add weight to this theory and identify a critical signaling molecule that may be key to the domino effect kicked off by nasal inflammation, a media release from FAU explains.

Study results suggest that application of an irritating component of a bacterium’s cell wall induces inflammation in the areas exactly where the olfactory neurons project, called the olfactory bulb. Moreover, these areas show the hallmark signs of PD, depositions of alpha-synuclein, the core components of Lewy bodies.

Inflammation Leads to Overexpression of Alpha-Synuclein

Quan and collaborators from China’s Xuzhou Medical University, Nanjing University of Information Science and Technology, and First Affiliated Hospital of Soochow University, demonstrate that inflammation induced in the nasal epithelium leads to overexpression of toxic forms of alpha-synuclein both in the olfactory system and in the dopamine neurons, which then degenerate and trigger Parkinson’s-like behaviors in mice. Using a mouse model developed by Quan, the researchers demonstrate that these effects require activation of a single receptor protein for the inflammatory signal, interleukin 1 beta. the release continues.

“Data from our study show that the bacterial trigger does not move across the blood-brain barrier. Rather, a sequential inflammatory activation of the olfactory mucosa triggers a subsequent expression of inflammatory molecules within the brain, propagating the inflammation.”

— Ning Quan, PhD

“Parkinson’s disease is a devastating neurodegenerative disorder. Currently, there is no cure for the disease and current medications have significant side-effects. These new findings may ultimately lead to potential therapies that could shut down the origins and progression of this debilitating disease.”

— Randy Blakely, PhD, executive director of FAU’s I-BRAIN

[Source(s): Florida Atlantic University, EurekAlert]