Aging increases the risk of Parkinson's disease (PD), making the disease more likely to occur at an older age. It is unclear how biological changes that accompany normal aging are related to changes leading to age-related diseases, such as Parkinson's. It is clear, however, that age-related chronic inflammation, known as inflammaging, is crucial to the onset of age-related diseases.
We aim to understand how biological changes that accompany aging cause inflammaging and how these changes promote the spread of alpha-synuclein -- a sticky protein that clumps in the brains of people with PD -- and the damage of brain cells in Parkinson's.
In this study, we will use existing blood samples from people with PD and from healthy people who are 100 and older. To accomplish the goals of this study, we will test the samples for the presence of molecules that induce or suppress inflammation, an approach called molecular panel testing. We will measure these molecules in the blood as well as DNA changes not related to the structure of genes (known as epigenetic changes) to determine the biological age of these people and identify any aging-related processes. To identify changes in protein glycosylation -- protein modifications that trigger inflammaging -- we will measure N-glycomic protein modifications in the blood samples.
Impact on Diagnosis/Treatment of Parkinson's disease:
We aim to better understand the processes leading to Parkinson's, identify possible diagnostic biomarkers (objective measures of disease) in the blood and also suggest new concepts for the development of neuroprotective therapies.
Next Steps for Development:
Upon completion of this study, we will propose a panel of molecular markers, i.e., a list of molecules that play a role in PD. The accuracy and usefulness of this panel should be confirmed in future studies. Once validated, this panel could be used in clinical trials of neuroprotective therapies.