Airborne Pollutants as Triggers of Parkinson's Disease via the Olfactory System

ABSTRACT

We are interested in determining whether ambient air pollutants impact the development of Parkinson's disease (PD) by increasing -synuclein pathology via inflammation. After completing Specific Aim 2, wherein we found no differences between experimental groups in spread of -syn, nor the expected nPM-induced neuroinflammatory changes. We repeated Specific Aim 2 mouse experiments with a new batch of nPM that showed in vitro activity. We collected tissues during the first week of SARS-CoV-2 quarantine. After restrictions were relaxed, we began analyzing tissues for neuroinflammation. This on-going analysis has yet to show strong inflammatory effects of the in vivo nPM exposure. Due to continued pandemic quarantine and travel restrictions we are discussing option with our collaborators. We will plan and execute novel experiments to explore the effects of LPS-induced olfactory inflammation on spread of -syn by histological (VAI) and biochemical (USC) analyses. We are interested in determining whether ambient air pollutants impact the development of Parkinson's disease (PD) by increasing -synuclein pathology via inflammation. After completing Specific Aim 2, wherein we found no differences between experimental groups in spread of -syn, nor the expected nPM-induced neuroinflammatory changes. We repeated Specific Aim 2 mouse experiments with a new batch of nPM that showed in vitro activity. We collected tissues during the first week of SARS-CoV-2 quarantine. After restrictions were relaxed, we began analyzing tissues for neuroinflammation. This on-going analysis has yet to show strong inflammatory effects of the in vivo nPM exposure. Due to continued pandemic quarantine and travel restrictions we are discussing option with our collaborators. We will plan and execute novel experiments to explore the effects of LPS-induced olfactory inflammation on spread of -syn by histological (VAI) and biochemical (USC) analyses.