The contribution of type-I IFN-mediated neuroinflammation to Parkinson's disease progression

TL;DR

This paper reviews how type-I interferons and microglia contribute to neuroinflammation in Parkinson's disease, potentially offering new therapeutic targets.

Contribution

The paper highlights the novel role of type-I interferon signaling in driving neuroinflammation and disease progression in Parkinson's.

Findings

Type-I interferons are linked to increased neuroinflammation in Parkinson's disease.

Microglia play a central role in propagating neuroinflammation through type-I interferon signaling.

Targeting type-I interferon signaling may slow Parkinson's disease progression.

Abstract

Parkinson's disease (PD) is a chronic neurodegenerative disease characterized by motor dysfunction. Pathological hallmarks of the disease include selective dopaminergic neuronal death, intraneuronal deposits known as Lewy bodies and extensive neuroinflammation within the central nervous system (CNS). Microglia are the key cellular players in mediating this neuroinflammatory response, propagating this neuropathology to exacerbate the neuronal cell death. Growing evidence suggests a role for the type-I interferons (IFN) in driving the neuroinflammatory response in PD, with increased type-I IFN signatures reported in both PD patients and in animal models of the disease. This review will discuss 1) the key players that modulate the neuroinflammatory response in PD and their implications in the CNS 2) the contribution of the type-I IFNs in driving the neuroinflammatory response in PD, and 3) evidence for therapeutically targeting type-I IFN signalling to slow disease progression. A greater understanding of the underlying mechanisms that lead to the elevated neuroinflammatory response in PD could lead to new advances in therapeutic targets that effectively slow the disease progression.

•Summarises how type-I interferon signalling contributes to Parkinson’s disease progression via innate immune activation.•Describes how type-I interferons and microglia drive chronic neuroinflammation and pathology in Parkinson’s disease.•Reviews neuroinflammation in Parkinson’s disease with emphasis on the role of type-I interferons in CNS immune dysregulation.

Summarises how type-I interferon signalling contributes to Parkinson’s disease progression via innate immune activation.

Describes how type-I interferons and microglia drive chronic neuroinflammation and pathology in Parkinson’s disease.

Reviews neuroinflammation in Parkinson’s disease with emphasis on the role of type-I interferons in CNS immune dysregulation.

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