Researchers believe that olfactory dysfunction may have a more direct linkage to the generation of Parkinson’s disease (PD). Formation of a protein called alpha-synuclein form Lewy bodies that can be located in olfactory areas and dopamine neurons whose loss triggers PD. Additionally, mutations in the gene encoding alpha-synuclein produce PD.
The sensory neurons that line the nasal epithelium are susceptible to neuroinflammatory attack due to their accessibility to environmental toxin exposure and toxins from bacteria, viruses and mold. These toxins can lead to local inflammatory responses in the nose where olfactory neurons send their sensitive endings and inflammation can spread to promote activation of inflammatory cells called microglia deeper in the brain.
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. Ning Quan, Ph.D., a neuroscientist from Florida Atlantic University's Schmidt College of Medicine and a faculty member of the FAU Brain Institute (I-BRAIN), is one of the researchers who published their results in the journal, Brain Pathology.
Quan and collaborators from China's Xuzhou Medical University, Nanjing University of Information Science and Technology, and First Affiliated Hospital of Soochow University, showed 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.
"Data from our study show that the bacterial trigger does not move across the blood-brain barrier," said Quan. "Rather, a sequential inflammatory activation of the olfactory mucosa triggers a subsequent expression of inflammatory molecules within the brain, propagating the inflammation."
Novel Study Links Chronic Inflammation in the Nose to Parkinson’s Disease