Abstract

An increasing number of genetic studies suggest that the pathogenesis of Parkinson’s disease (PD) and cancer share common genes, pathways, and mechanisms. Despite a disruption in a wide range of similar biological processes, the end result is very different: uncontrolled proliferation and early neurodegeneration. Thus, the links between the molecular mechanisms that cause PD and cancer remain to be elucidated. We propose that chronic inflammation in neurons and tumors contributes to a microenvironment that favors the accumulation of DNA mutations and facilitates disease formation. This article appraises the key role of microglia, establishes the genetic role of COX2 and CARD15 in PD and cancer, and discusses prevention and treatment with this new perspective in mind. We examine the evidence that chronic inflammation is an important link between cancer and PD.

Highlights

  • The three early, typical symptoms of Parkinson’s disease (PD) are static tremors, muscle rigidity, and bradykinesia, which result from the degeneration of dopaminergic neurons in the midbrain

  • It was suggested that PD patients with a low incidence of cancer may be associated with the negative correlation between PD and smoking (Hernan et al, 2002)

  • The reduced risk of smoking-related cancers can be explained in PD patients, it cannot decipher the risk of nonsmoking-related cancers

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Summary

INTRODUCTION

The three early, typical symptoms of Parkinson’s disease (PD) are static tremors, muscle rigidity, and bradykinesia, which result from the degeneration of dopaminergic neurons in the midbrain. Case-controlled and large prospective studies reported a lower rate of smoking-related and non-smoking-related cancers in PD patients. Thyroid, and breast cancer were revealed to have an increased incidence in PD patients (D’Amelio et al, 2009; Liu et al, 2011). One of theories between PD and skin cancer may be associated with the mode of therapy, such as Levodopa, rather than with the disease itself (Paisan-Ruiz and Houlden, 2010). It was suggested that PD patients with a low incidence of cancer may be associated with the negative correlation between PD and smoking (Hernan et al, 2002). Genetic studies provide additional understanding, since many familial PD genes have been associated with cancer, such as parkin (PARK2), PINK1 (PARK6), DJ-1 (PARK7), and LRRK2 (PARK8; Table 1).

Inheritance Expression in cancer in PD
PROVEN GENETIC RISK IMPLICATED IN BOTH CANCER AND PD
THERAPEUTIC INTERVENTIONS INSPIRED BY THEIR LINKS
Findings
CONCLUSION
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