Abstract

To the Editor,
Psoriasis and Parkinson’s disease (PD) are enduring conditions that can significantly impact the physical and mental well-being of individuals affected by them. Despite their apparent dissimilarity in symptoms, underlying mechanisms, and medical specialties, prior research has suggested a potential link between these conditions. 1 We set out to explore the existing literature to analyze overlapping inflammatory pathways, genetic susceptibilities, or systematic dysregulations that exist in patients with both conditions.
A search of OVID’s Medline and Embase databases was completed from inception of July 2, 2023, according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR). A summary of the findings from the included literature can be found in Supplemental Table 1. The full search strategy is provided in Supplemental Table 2, as well as the articles included (Supplemental Figure 1).
Several studies have reported a positive, statistically significant correlation between the concomitant development of PD and psoriasis. 1 However, conflicting findings exist, with some studies finding weak or no association. 2,3 As such, the relationship between prevalence and disease progression remains controversial. Notably, treatment may influence this relationship as systemic therapy for psoriasis has been found to reduce PD risk. 4
Similarly, there is not currently a consensus on the physiological connection between PD and psoriasis, however there are several pathogenic links between the diseases, including inflammation pathways, oxidative stress, metabolic disorders, and genetic factors. 3 Several studies have pointed to proinflammatory mediators and various inflammatory pathways as a potential connection between PD and psoriasis. It was found that patients with chronic autoimmune disease have an increased risk of developing neurodegenerative diseases, including PD. 1 Additionally, it has been suggested that patients with psoriasis have an increased risk of developing PD due to a chronic state of inflammation, which can induce microglial activation and the release of reactive oxygen species, resulting in neuronal damage. 1,5
An important consideration raised by literature includes the role of obesity in the relationship between PD and psoriasis. 5 Obesity is a risk factor for the development of PD, and a recent study has found that a high body mass index increases the risk of PD in a dose-dependent manner. 1 Additionally, there is a strong correlation between obesity and psoriasis. It has been hypothesized that in obese patients, adipose tissue dysregulation results in the production of cytokines and bioactive products including interleukin-6, leptin, resistin, and TNF-a, all of which may increase the risk of developing psoriasis. 5 With both PD and psoriasis being inflammatory diseases, the proposal of one or numerous shared proinflammatory pathways is plausible. As obesity is associated with both PD and psoriasis independently, the relationship between the two diseases may be confounded by obesity. 1
The association between psoriasis and PD is a topic of ongoing investigation, with conflicting findings in existing literature. This scoping review provides a foundation for future studies aiming to establish a clear connection between these conditions. Further research is needed to address the risk in clinical practice for enhanced diagnosis, treatment, and patient outcomes.
Supplemental Material
Supplementary Material 1 - Supplemental material for Association Between Parkinson’s Disease and Psoriasis: A Scoping Review
Supplemental material, Supplementary Material 1, for Association Between Parkinson’s Disease and Psoriasis: A Scoping Review by Dea Metko, Nicol Vaizman, Shanti Mehta and Ronald Vender in Journal of Cutaneous Medicine and Surgery
Footnotes
Declaration of Conflicting Interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The authors received no financial support for the research, author-ship, and/or publication of this article.
Supplemental Material
Supplemental material for this article is available online.
References
Supplementary Material
Please find the following supplemental material available below.
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