Authors:

Jacob Gold

Date Created:

Not specified

Course Title:

Professor:

Not specified

About Paper:

Parkinson's disease (PD) is a neurodegenerative disorder characterized by a loss of dopaminergic neurons in the substantia nigra region of the midbrain, as well as the formation of Lewy body inclusions enriched with aggregated forms of the protein alpha-synuclein (aSyn) throughout the brain. The propagation of Lewy bodies across interconnected brain regions, a process that is apparently promoted by oxidative stress, is thought to play a key role in the pathogenesis and progression of PD. Polyphenols, a group of phytochemicals present in various foods and medicines, have drawn much attention for their ability to alleviate oxidative stress. Previous research has characterized the neuroprotective role of polyphenols in toxicant PD models, focusing on amelioration of the oxidative stress component of PD. Additionally, some polyphenols have been examined for their ability to inhibit aSyn aggregation. Here, we aim to further characterize the relationship between polyphenols and aSyn pathology by utilizing a cellular model of PD that recapitulates the propagation of aSyn aggregates described above. In this model, HEK293T cells overexpressing aSyn tagged with a fluorescent protein are treated with aSyn pre-formed fibrils (PFFs) and monitored for evidence of seeded aSyn aggregation by confocal microscopy. We hypothesize that cells co-treated with PFFs and polyphenols will show a reduced aSyn aggregate burden, consistent with the idea that polyphenols can interfere with the propagation of aSyn pathology. This project provides a basis for further investigation of polyphenols as potential disease-modifying therapeutics for PD. Keywords: Alpha-Synuclein; Parkinson's Disease; Neurodegeneration; Polyphenol; Protein Aggregation

Source:

Purdue University / 2024

Topics:

No topics listed

Co-authors:

Jacob Gold