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Dear Colleagues,

There is an unmet medical need for therapeutic interventions in Parkinson’s disease (PD) that can change the course of this devastating disorder, either by slowing or halting the progression of symptoms. Even though the etiology of PD is multifactorial and not well defined, scientific advancements in PD biology and genetics allowed the identification of rare genetic mutations and gene variants that cause or increase the risk for PD. The study of these genes and their products, such as alpha-synuclein, LRRK2 and glucocerebrosidase, provided insight into molecular pathways underlying PD pathogenesis. Moreover, neuroinflammation is now recognized as an important factor in the neurodegenerative processes of PD.

The aim of this Special Issue entitled “Emerging Therapeutic Targets for Parkinson’s Disease” is to provide a platform for presenting updates and the latest research on therapeutic interventions that are targeting disease pathways, currently under clinical evaluation or that hold promise for future assessment. We invite authors to contribute with review or original research articles focusing on promising therapeutic approaches, presenting evidence from preclinical disease-relevant models, or discussing the benefits and the continuing challenges that these targets present.

Dr. Elpida Tsika
Guest Editor

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Keywords

alpha-synuclein
glucocerebrosidase
LRRK2
familial Parkinson’s disease
neuroinflammation
lysosomal - autophagy pathway
mitochondrial function

Published Papers (2 papers)

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Review

29 pages, 3735 KiB

Open AccessReview

The Footprint of Kynurenine Pathway in Neurodegeneration: Janus-Faced Role in Parkinson’s Disorder and Therapeutic Implications

by Tapan Behl, Ishnoor Kaur, Aayush Sehgal, Sukhbir Singh, Saurabh Bhatia, Ahmed Al-Harrasi, Gokhan Zengin, Adrian Gheorghe Bumbu, Felicia Liana Andronie-Cioara, Aurelia Cristina Nechifor, Daniela Gitea, Alexa Florina Bungau, Mirela Marioara Toma and Simona Gabriela Bungau

Int. J. Mol. Sci. 2021, 22(13), 6737; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22136737 - 23 Jun 2021

Cited by 21 | Viewed by 4386

Abstract

Progressive degeneration of neurons and aggravation of dopaminergic neurons in the substantia nigra pars compacta results in the loss of dopamine in the brain of Parkinson’s disease (PD) patients. Numerous therapies, exhibiting transient efficacy have been developed; however, they are mostly accompanied by side effects and limited reliability, therefore instigating the need to develop novel optimistic treatment targets. Significant therapeutic targets have been identified, namely: chaperones, protein Abelson, glucocerebrosidase-1, calcium, neuromelanin, ubiquitin-proteasome system, neuroinflammation, mitochondrial dysfunction, and the kynurenine pathway (KP). The role of KP and its metabolites and enzymes in PD, namely quinolinic acid (QUIN), kynurenic acid (KYNA), 3-hydroxykynurenine (3-HK), 3-hydroxyanthranillic acid (3-HAA), kunurenine-3-monooxygenase (KMO), etc. has been reported. The neurotoxic QUIN, N-methyl-D-aspartate (NMDA) receptor agonist, and neuroprotective KYNA—which antagonizes QUIN actions—primarily justify the Janus-faced role of KP in PD. Moreover, KP has been reported to play a biomarker role in PD detection. Therefore, the authors detail the neurotoxic, neuroprotective, and immunomodulatory neuroactive components, alongside the upstream and downstream metabolic pathways of KP, forming a basis for a therapeutic paradigm of the disease while recognizing KP as a potential biomarker in PD, thus facilitating the development of a suitable target in PD management. Full article

(This article belongs to the Special Issue Emerging Therapeutic Targets for Parkinson's Disease)

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13 pages, 738 KiB

Open AccessReview

Potential Effects of Leukotriene Receptor Antagonist Montelukast in Treatment of Neuroinflammation in Parkinson’s Disease

by Johan Wallin and Per Svenningsson

Int. J. Mol. Sci. 2021, 22(11), 5606; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22115606 - 25 May 2021

Cited by 12 | Viewed by 4174

Abstract

Parkinson’s disease (PD) is a neurodegenerative disorder where misfolded alpha-synuclein-enriched aggregates called Lewy bodies are central in pathogenesis. No neuroprotective or disease-modifying treatments are currently available. Parkinson’s disease is considered a multifactorial disease and evidence from multiple patient studies and animal models has shown a significant immune component during the course of the disease, highlighting immunomodulation as a potential treatment strategy. The immune changes occur centrally, involving microglia and astrocytes but also peripherally with changes to the innate and adaptive immune system. Here, we review current understanding of different components of the PD immune response with a particular emphasis on the leukotriene pathway. We will also describe evidence of montelukast, a leukotriene receptor antagonist, as a possible anti-inflammatory treatment for PD. Full article

(This article belongs to the Special Issue Emerging Therapeutic Targets for Parkinson's Disease)

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