Shedding light on thyroid hormone disorders and Parkinson disease pathology: mechanisms and risk factors

Mohammadi, Soheil; Dolatshahi, Mahsa; Rahmani, Farzaneh

doi:10.1007/s40618-020-01314-5

Cited by 50 publications

(39 citation statements)

References 116 publications

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“…Specifically, one study identified patients with hypothyroidism to have a two-fold elevated risk of developing PD 63 . Collectively, these findings support the growing body of evidence for the importance of the oesophagus 64,65 and thyroid 62 in PD.…”

Section: Discussionsupporting

confidence: 79%

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Establishing gene regulatory networks from Parkinson’s disease risk loci

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Schierding

Gokuladhas

et al. 2021

Preprint

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The latest meta-analysis of genome wide association studies (GWAS) identified 90 independent single nucleotide polymorphisms (SNPs) across 78 genomic regions associated with Parkinson's disease (PD), yet the mechanisms by which these variants influence the development of the disease remains largely elusive. To establish the functional gene regulatory networks associated with PD-SNPs, we utilised an approach combining spatial (chromosomal conformation capture) and functional (expression quantitative trait loci; eQTL) data. We identified 518 genes subject to regulation by 76 PD-SNPs across 49 tissues, that encompass 36 peripheral and 13 CNS tissues. Notably, one third of these genes were regulated via trans- acting mechanisms (distal; risk locus-gene separated by > 1Mb, or on different chromosomes). Of particular interest is the identification of a novel trans-eQTL-gene connection between rs10847864 and SYNJ1 in the adult brain cortex, highlighting a convergence between familial studies and PD GWAS loci for SYNJ1 (PARK20) for the first time. Furthermore, we identified 16 neuro-development specific eQTL-gene regulatory connections within the foetal cortex, consistent with hypotheses suggesting a neurodevelopmental involvement in the pathogenesis of PD. Through utilising Louvain clustering we extracted nine significant and highly intra-connected clusters within the entire gene regulatory network. The nine clusters are enriched for specific biological processes and pathways, some of which have not previously been associated with PD. Together, our results not only contribute to an overall understanding of the mechanisms and impact of specific combinations of PD-SNPs, but also highlight the potential impact gene regulatory networks may have when elucidating aetiological subtypes of PD.

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Section: Discussionsupporting

confidence: 79%

“…Secondly, we identified the thyroid tissue as being enriched for eQTLs, many of which were not represented in CNS tissues. The thyroid is a component of the dopaminergic system and hypothalamic-pituitary-thyroid axis network 61 . A potential link between thyroid hormone disorders, PD risk, and symptom severity has been suggested 62 .…”

Section: Discussionmentioning

confidence: 99%

Establishing gene regulatory networks from Parkinson’s disease risk loci

Farrow

Schierding

Gokuladhas

et al. 2021

Preprint

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“…Extrapolation can also be made from SARS CoV-1 data since in previous autopsy studies SARS-CoV-1 was responsible for follicular cell destruction, extensive apoptosis, and fibrosis in the absence of lymphocytic infiltration, representing the histopathological hallmarks of destructive thyroiditis [ 71 ]. Alternatively, thyroid inflammation might be caused by the cytokine storm associated with COVID-19, as above reported [ 14 ]. In the acute phase, increased concentrations of pro-inflammatory cytokines, and in particular of IL-6, may trigger thyroiditis and related thyrotoxicosis, the prevalence of which has been shown to correlate with IL-6 elevation [ 34 , 72 ].…”

Section: Destructive Thyrotoxicosis In Covid-19 Patientsmentioning

confidence: 87%

SARS-COV-2-related immune-inflammatory thyroid disorders: facts and perspectives

Ruggeri

Campennì

Deandreis

et al. 2021

Expert Review of Clinical Immunology

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Introduction : During the COVID-19 pandemic thyroid gland alteration/dysfunction has been emerged as a possible endocrine complication. The present review is focused on inflammatory and autoimmune thyroid complications triggered by SARS-CoV-2 infection by searching through databases like MEDLINE and Scopus up to April 2021. Areas covered : Beside the occurrence of ‘non-thyroidal illness’ in severe clinical conditions, alterations of thyroid function and structure may occur during COVID-19 as a consequence of either direct or indirect effects of SARS-CoV-2 infection on the gland. On the one hand, SARS-CoV-2 uses ACE2 as a receptor to infect the host cells and ACE2 is highly expressed by follicular thyroid cells. On the other hand, COVID-19 is associated with a systemic inflammatory and immune response, involving Th1/Th17/Th2 lymphocytes and proinflammatory cytokines, which resembles the immune activation that occurs in immune-mediated thyroid diseases. COVID-19-related thyroid disorders include destructive thyroiditis and onset or relapse of autoimmune thyroid disorders, leading to a broad spectrum of thyroid dysfunction ranging from thyrotoxicosis to hypothyroidism, that may worsen COVID-19 clinical course and affect prognosis. Expert opinion : Physicians should be aware of the possible occurrence of thyroid dysfunction during and after SARS-CoV-2 infection. Further longitudinal studies are warranted to evaluate potential long-term sequelae.

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“…The interaction(s) between vitamin D and its role in general immune status (as well as specific associations with COVID-19 severity) merit further studies. Early research results on these purported associations support further exploration of this potential factor on disease outcomes and virulence [ 16 , 17 , 18 , 19 ]. Moreover, associations between COVID-19 mortality and diet/lifestyle factors, such as nutritional status or consumption of seafood, warrant further exploration.…”

Section: Discussionmentioning

confidence: 93%

Spatial Variability in COVID-19 Mortality

Bossak

Turk

2021

IJERPH

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COVID-19 emerged as a global pandemic in the spring of 2020. Since that time, the disease has resulted in approximately 150 million cases and 3 million deaths worldwide. However, there is significant spatial variation in the rate of mortality from COVID-19. Here, we briefly explore spatial variations in COVID-19 mortality by country groupings and propose possible explanations for the differences observed. Specifically, we find that there is a statistically significant difference in COVID-19 mortality between countries grouped into categories based on (1) developed, primarily western diets and healthcare systems; (2) “Scandinavian” countries with advanced healthcare systems and generally anti-inflammatory diets, and (3) developing countries. We do not infer causality but believe that the observed associations provide hypotheses for future research investigations. Moreover, our results add further evidence to support additional exploration of vitamin D exposure/status and COVID-19 mortality.

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Shedding light on thyroid hormone disorders and Parkinson disease pathology: mechanisms and risk factors

Cited by 50 publications

References 116 publications

Establishing gene regulatory networks from Parkinson’s disease risk loci

Establishing gene regulatory networks from Parkinson’s disease risk loci

SARS-COV-2-related immune-inflammatory thyroid disorders: facts and perspectives

Spatial Variability in COVID-19 Mortality

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