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Updated: Jun 19, 2026

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

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Published on: January 5, 2016

Multiomic Analysis Reveals Molecular Pathways Associated with Intestinal Aggregation of α-Synuclein.

Julia M Balsamo¹, Ying Yan², Dylan Thai¹

¹Department of Chemistry, University of California, Irvine, California 92617, United States.

ACS Chemical Biology

|January 2, 2026

Summary

Parkinson's disease may start in the gut. Nitrite exposure triggers alpha-synuclein aggregation in gut cells, which can spread to the brain. Dopamine pathway inhibitors show promise in preventing this aggregation.

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Published on: November 25, 2022

Area of Science:

Neuroscience
Gastroenterology
Biochemistry

Background:

Parkinson's disease (PD) is linked to alpha-synuclein aggregation, potentially originating in the gut.
Enteroendocrine cells in the gut express alpha-synuclein and interact with the nervous system.
Gut microbiota metabolites, like nitrite, can induce alpha-synuclein aggregation in these cells.

Purpose of the Study:

To elucidate the cellular and molecular mechanisms of nitrite-induced alpha-synuclein aggregation in enteroendocrine cells.
To investigate the role of dopamine in this aggregation process.
To explore potential therapeutic strategies targeting gut-initiated PD.

Main Methods:

Untargeted proteomics of nitrite-exposed enteroendocrine cells.
Targeted analysis of dopamine's role in alpha-synuclein aggregation.
Lipidome profiling of enteroendocrine cells.
Assessment of cell viability under stress conditions.

Main Results:

Nitrite exposure initiates alpha-synuclein aggregation in enteroendocrine cells via specific pathways.
Dopamine is critical for nitrite-induced aggregation; its absence suppresses aggregation.
Enteroendocrine cells exhibit robustness, potentially serving as reservoirs for aggregates.
Inhibitors of dopamine biosynthesis (benserazide, alpha-methyl tyrosine) reduced aggregation.

Conclusions:

Enteroendocrine cells are key players in the gut-initiated cascade of Parkinson's disease.
Dopamine metabolism is a critical target for preventing alpha-synuclein aggregation in the gut.
Further research into lipid metabolism in PD is warranted.
These findings support the development of therapies to prevent gut-to-brain alpha-synuclein spread.