Protein Translation in the Pathogenesis of Parkinson’s Disease

TL;DR

This paper explores how protein translation, often overlooked in Parkinson’s disease research, may play a key role in its development and progression.

Contribution

The paper highlights the emerging role of protein translation in Parkinson’s disease pathogenesis, beyond traditional proteostasis mechanisms.

Findings

Dysregulation of protein translation is linked to Parkinson’s disease and other neurodegenerative disorders.

Aggregates in Parkinson’s disease may directly influence protein translation, worsening neuronal stress.

Understanding translation’s role could lead to new diagnostics and therapeutics for Parkinson’s disease.

Abstract

In recent years, research into Parkinson’s disease and similar neurodegenerative disorders has increasingly suggested that these conditions are synonymous with failures in proteostasis. However, the spotlight of this research has remained firmly focused on the tail end of proteostasis, primarily aggregation, misfolding, and degradation, with protein translation being comparatively overlooked. Now, there is an increasing body of evidence supporting a potential role for translation in the pathogenesis of PD, and its dysregulation is already established in other similar neurodegenerative conditions. In this paper, we consider how altered protein translation fits into the broader picture of PD pathogenesis, working hand in hand to compound the stress placed on neurons, until this becomes irrecoverable. We will also consider molecular players of interest, recent evidence that suggests that aggregates may directly influence translation in PD progression, and the implications for the role of protein translation in our development of clinically useful diagnostics and therapeutics.

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