Parkinson’s Disease as a Risk Factor for Melanoma: A Review

Objective: To review the literature and place into a quantified context the relationship of Parkinson’s disease diagnosis to a subsequent diagnosis of malignant melanoma, and to briefly explore potential molecular associations between the two diseases. Methods: The Medline database was queried with terms related to Parkinson’s disease (PD) and malignant melanoma, with use of Boolean operator AND to identify studies involving both diseases. Studies were divided into primary and meta-analyses, with exclusive evaluation of those quantifying risk of malignant melanoma after an established diagnosis of Parkinson’s disease. Critical studies were identified using Medline searches to identify established quantified risk metrics between classic melanoma risk factors and subsequent development of malignant melanoma. Results: Twelve primary studies and three meta-analyses were evaluated and their risk metrices tabulated. Three studies offered estimated risk of development of malignant melanoma in patients with classic melanoma risk factors. These metrices were also tabulated and compared with the metrices established by the twelve primary studies. This demonstrated a similarity in overall risk of developing malignant melanoma in a patient with a diagnosis of Parkinson’s disease as compared to a patient with classical melanoma risk factors. Limitations: Relatively few studies identified specifically quantified the classic risk factors for melanoma, and relatively few studies specifically quantified the degree of risk for developing melanoma after an established Parkinson’s disease diagnosis. Conclusion: It is wise to consider the presence of Parkinson’s disease in a patient as one factor when clinicians decide on the appropriateness of regular full body screening examinations.

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Environmental risk factors and Parkinson's disease: An umbrella review of meta-analyses

Parkinsonism & Related Disorders ◽

10.1016/j.parkreldis.2015.12.008 ◽

2016 ◽

Vol 23 ◽

pp. 1-9 ◽

Cited By ~ 139

Author(s):

Vanesa Bellou ◽

Lazaros Belbasis ◽

Ioanna Tzoulaki ◽

Evangelos Evangelou ◽

John P.A. Ioannidis

Keyword(s):

Risk Factors ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Environmental Risk ◽

Environmental Risk Factors ◽

Umbrella Review ◽

Meta Analyses

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A systematic review of nutritional risk factors of Parkinson's disease

Nutrition Research Reviews ◽

10.1079/nrr2005108 ◽

2005 ◽

Vol 18 (2) ◽

pp. 259-282 ◽

Cited By ~ 28

Author(s):

Lianna Ishihara ◽

Carol Brayne

Keyword(s):

Risk Factors ◽

Systematic Review ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cohort Studies ◽

Meta Analysis ◽

Caffeine Intake ◽

Inverse Association ◽

Coffee Drinking ◽

Meta Analyses

A wide variety of nutritional exposures have been proposed as possible risk factors for Parkinson's disease (PD) with plausible biological hypotheses. Many studies have explored these hypotheses, but as yet no comprehensive systematic review of the literature has been available. MEDLINE, EMBASE, and WEB OF SCIENCE databases were searched for existing systematic reviews or meta-analyses of nutrition and PD, and one meta-analysis of coffee drinking and one meta-analysis of antioxidants were identified. The databases were searched for primary research articles, and articles without robust methodology were excluded by specified criteria. Seven cohort studies and thirty-three case–control (CC) studies are included in the present systematic review. The majority of studies did not find significant associations between nutritional factors and PD. Coffee drinking and alcohol intake were the only exposures with a relatively large number of studies, and meta-analyses of each supported inverse associations with PD. Factors that were reported by at least one CC study to have significantly increased consumption among cases compared with controls were: vegetables, lutein, xanthophylls, xanthins, carbohydrates, monosaccharides, junk food, refined sugar, lactose, animal fat, total fat, nuts and seeds, tea, Fe, and total energy. Factors consumed significantly less often among cases were: fish, egg, potatoes, bread, alcohol, coffee, tea, niacin, pantothenic acid, folate and pyridoxine. In three cohort studies, two reported borderline decreased relative risks and one a significant increased risk with vitamin C intake. One cohort reported an inverse association between caffeine intake and PD. Three cohorts reported significant positive association in men between dairy products and PD.

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ADORA2A rs5760423 and CYP1A2 rs762551 Polymorphisms as Risk Factors for Parkinson’s Disease

Journal of Clinical Medicine ◽

10.3390/jcm10030381 ◽

2021 ◽

Vol 10 (3) ◽

pp. 381 ◽

Cited By ~ 1

Author(s):

Vasileios Siokas ◽

Athina-Maria Aloizou ◽

Zisis Tsouris ◽

Ioannis Liampas ◽

Panagiotis Liakos ◽

...

Keyword(s):

Risk Factors ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Genetic Basis ◽

Genetic Model ◽

Healthy Controls ◽

Exact Role ◽

Negative Results ◽

Meta Analyses

Background: Parkinson’s disease (PD) is the second commonest neurodegenerative disease. The genetic basis of PD is indisputable. Both ADORA2A rs5760423 and CYP1A2 rs762551 have been linked to PD, to some extent, but the exact role of those polymorphisms in PD remains controversial. Objective: We assessed the role of ADORA2A rs5760423 and CYP1A2 rs762551 on PD risk. Methods: We genotyped 358 patients with PD and 358 healthy controls for ADORA2A rs5760423 and CYP1A2 rs762551. We also merged and meta-analyzed our data with data from previous studies, regarding these two polymorphisms and PD. Results: No significant association with PD was revealed (p > 0.05), for either ADORA2A rs5760423 or CYP1A2 rs762551, in any of the examined genetic model of inheritance. In addition, results from meta-analyses yield negative results. Conclusions: Based on our analyses, it appears rather unlikely that ADORA2A rs5760423 or CYP1A2 rs762551 is among the major risk factors for PD, at least in Greek patients with PD.

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SPECT and fMRI analysis of motor and cognitive indices of early Parkinson's disease: The relationship of striatal dopamine and cortical function

PsycEXTRA Dataset ◽

10.1037/e446682006-001 ◽

2000 ◽

Author(s):

John D. E. Gabrieli

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Striatal Dopamine ◽

Cortical Function ◽

Fmri Analysis ◽

Relationship Of ◽

The Relationship ◽

Early Parkinson’S Disease

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ROLE OF ENVIRONMENTAL RISK FACTORS IN PARKINSON'S DISEASE: BUCOVINA REGION CASE STUDY

Environmental Engineering and Management Journal ◽

10.30638/eemj.2015.260 ◽

2015 ◽

Vol 14 (10) ◽

pp. 2435-2444

Author(s):

Oana Geman ◽

Hariton Costin

Keyword(s):

Risk Factors ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Environmental Risk ◽

Environmental Risk Factors

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Faculty Opinions recommendation of Baseline predictors for progression 4 years after Parkinson's disease diagnosis in the De Novo Parkinson Cohort (DeNoPa).

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.734486834.793553765 ◽

2018 ◽

Author(s):

Joseph Jankovic ◽

Arjun Tarakad

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

De Novo ◽

Disease Diagnosis

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Putative second hit rare genetic variants in families with seemingly GBA-associated Parkinson’s disease

npj Genomic Medicine ◽

10.1038/s41525-020-00163-8 ◽

2021 ◽

Vol 6 (1) ◽

Author(s):

Muhammad Aslam ◽

Nirosiya Kandasamy ◽

Anwar Ullah ◽

Nagarajan Paramasivam ◽

Mehmet Ali Öztürk ◽

...

Keyword(s):

Risk Factors ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Genetic Variants ◽

Rare Variants ◽

Alpha Synuclein ◽

Younger Age ◽

Targeted Treatments ◽

Genes Encoding ◽

Rare Genetic Variants

AbstractRare variants in the beta-glucocerebrosidase gene (GBA1) are common genetic risk factors for alpha synucleinopathy, which often manifests clinically as GBA-associated Parkinson’s disease (GBA-PD). Clinically, GBA-PD closely mimics idiopathic PD, but it may present at a younger age and often aggregates in families. Most carriers of GBA variants are, however, asymptomatic. Moreover, symptomatic PD patients without GBA variant have been reported in families with seemingly GBA-PD. These observations obscure the link between GBA variants and PD pathogenesis and point towards a role for unidentified additional genetic and/or environmental risk factors or second hits in GBA-PD. In this study, we explored whether rare genetic variants may be additional risk factors for PD in two families segregating the PD-associated GBA1 variants c.115+1G>A (ClinVar ID: 93445) and p.L444P (ClinVar ID: 4288). Our analysis identified rare genetic variants of the HSP70 co-chaperone DnaJ homolog subfamily B member 6 (DNAJB6) and lysosomal protein prosaposin (PSAP) as additional factors possibly influencing PD risk in the two families. In comparison to the wild-type proteins, variant DNAJB6 and PSAP proteins show altered functions in the context of cellular alpha-synuclein homeostasis when expressed in reporter cells. Furthermore, the segregation pattern of the rare variants in the genes encoding DNAJB6 and PSAP indicated a possible association with PD in the respective families. The occurrence of second hits or additional PD cosegregating rare variants has important implications for genetic counseling in PD families with GBA1 variant carriers and for the selection of PD patients for GBA targeted treatments.

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