What Can Inflammation Tell Us about Therapeutic Strategies for Parkinson's Disease?

Int J Mol Sci. 2024 Jan 29;25(3):1641. doi: 10.3390/ijms25031641.

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder with a complicated etiology and pathogenesis. α-Synuclein aggregation, dopaminergic (DA) neuron loss, mitochondrial injury, oxidative stress, and inflammation are involved in the process of PD. Neuroinflammation has been recognized as a key element in the initiation and progression of PD. In this review, we summarize the inflammatory response and pathogenic mechanisms of PD. Additionally, we describe the potential anti-inflammatory therapies, including nod-like receptor pyrin domain containing protein 3 (NLRP3) inflammasome inhibition, nuclear factor κB (NF-κB) inhibition, microglia inhibition, astrocyte inhibition, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibition, the peroxisome proliferator-activated receptor γ (PPARγ) agonist, targeting the mitogen-activated protein kinase (MAPK) pathway, targeting the adenosine monophosphate-activated protein kinase (AMPK)-dependent pathway, targeting α-synuclein, targeting miRNA, acupuncture, and exercise. The review focuses on inflammation and will help in designing new prevention strategies for PD.

Keywords: Parkinson’s disease; inflammation; mechanisms; therapies.

Publication types

  • Review

MeSH terms

  • Dopaminergic Neurons / metabolism
  • Humans
  • Inflammasomes / metabolism
  • Inflammation / metabolism
  • Microglia / metabolism
  • NLR Family, Pyrin Domain-Containing 3 Protein / metabolism
  • Neurodegenerative Diseases* / metabolism
  • Parkinson Disease* / metabolism
  • alpha-Synuclein / metabolism

Substances

  • alpha-Synuclein
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Inflammasomes