International Journal of Molecular Sciences

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Molecular Research in Parkinson's Disease

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Dear Colleagues,

This Special Issue aims to bring together cutting-edge research that will contribute to our collective efforts in deciphering the molecular underpinnings of Parkinson’s disease (PD) and exploring innovative therapeutic avenues.

PD is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, leading to motor and non-motor symptoms that severely impact patients' quality of life. Despite significant advancements, the precise molecular mechanisms driving PD remain elusive. The field of molecular research has made remarkable strides in identifying genetic, epigenetic, and biochemical factors involved in PD, providing new insights into disease pathogenesis and potential therapeutic targets.

This Special Issue will cover a wide range of topics within molecular research in PD, including but not limited to the following:

Genetic mutations and their role in familial and sporadic PD;
Epigenetic modifications and their impact on gene expression in PD;
Protein misfolding and aggregation, particularly α-synuclein pathology;
Mitochondrial dysfunction and oxidative stress in PD;
Neuroinflammation and its molecular mediators;
Advances in biomarker discovery for early diagnosis and disease progression;
Novel and advanced models for PD, such as animal models, organoids, induced pluripotent stem cells (iPSCs), and three-dimensional (3D) culture systems;
Novel therapeutic strategies targeting molecular pathways in PD.

We invite original research articles, reviews, short communications and other types of papers that provide significant contributions to the field of molecular research in PD. We look forward to receiving your contributions and to the impactful discussions that will emerge from this Special Issue. Together, we can advance our understanding of Parkinson's Disease and pave the way for innovative therapies that will improve the lives of those affected by this challenging condition.

Prof. Dr. Yi-Chuan Cheng
Guest Editor

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31 pages, 4060 KiB

Open AccessArticle

Brain-Region-Specific Differences in Protein Citrullination/Deimination in a Pre-Motor Parkinson’s Disease Rat Model

by Audrey Mercer, Marco Sancandi, Amy Maclatchy and Sigrun Lange

Int. J. Mol. Sci. 2024, 25(20), 11168; https://doi.org/10.3390/ijms252011168 - 17 Oct 2024

Viewed by 478

Abstract

The detection of early molecular mechanisms and potential biomarkers in Parkinson’s disease (PD) remains a challenge. Recent research has pointed to novel roles for post-translational citrullination/deimination caused by peptidylarginine deiminases (PADs), a family of calcium-activated enzymes, in the early stages of the disease. The current study assessed brain-region-specific citrullinated protein targets and their associated protein–protein interaction networks alongside PAD isozymes in the 6-hydroxydopamine (6-OHDA) induced rat model of pre-motor PD. Six brain regions (cortex, hippocampus, striatum, midbrain, cerebellum and olfactory bulb) were compared between controls/shams and the pre-motor PD model. For all brain regions, there was a significant difference in citrullinated protein IDs between the PD model and the controls. Citrullinated protein hits were most abundant in cortex and hippocampus, followed by cerebellum, midbrain, olfactory bulb and striatum. Citrullinome-associated pathway enrichment analysis showed correspondingly considerable differences between the six brain regions; some were overlapping for controls and PD, some were identified for the PD model only, and some were identified in control brains only. The KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways identified in PD brains only were associated with neurological, metabolic, immune and hormonal functions and included the following: “Axon guidance”; “Spinocerebellar ataxia”; “Hippo signalling pathway”; “NOD-like receptor signalling pathway”; “Phosphatidylinositol signalling system”; “Rap1 signalling pathway”; “Platelet activation”; “Yersinia infection”; “Fc gamma R-mediated phagocytosis”; “Human cytomegalovirus infection”; “Inositol phosphate metabolism”; “Thyroid hormone signalling pathway”; “Progesterone-mediated oocyte maturation”; “Oocyte meiosis”; and “Choline metabolism in cancer”. Some brain-region-specific differences were furthermore observed for the five PAD isozymes (PADs 1, 2, 3, 4 and 6), with most changes in PAD 2, 3 and 4 when comparing control and PD brain regions. Our findings indicate that PAD-mediated protein citrullination plays roles in metabolic, immune, cell signalling and neurodegenerative disease-related pathways across brain regions in early pre-motor stages of PD, highlighting PADs as targets for future therapeutic avenues. Full article

(This article belongs to the Special Issue Molecular Research in Parkinson's Disease)

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