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Parkinson's Disease, but Several, Perhaps Most, of Them May Reflect Reverse Causation, Residual Confounding, Information Bias, Sponsor Conflicts Or Other Caveats.”2

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Parkinson's Disease, but Several, Perhaps Most, of Them May Reflect Reverse Causation, Residual Confounding, Information Bias, Sponsor Conflicts Or Other Caveats.”2 Parkinson’s Disease Introduction Parkinson’s disease is a slowly progressive and degenerative movement disorder that is characterized by asymmetric resting tremor, rigidity, bradykinesia, gait instability, and postural instability. Of these characteristics, the most common initial motor symptom is a resting tremor in an upper extremity. The tremor is generally asymmetric. The major findings in Parkinson’s disease include the loss of dopaminergic neurons in the substantia nigra pars compacta and the presence of Lewy bodies; even so, there is no definitive test that can confirm a diagnosis of Parkinson’s disease during a person's life. As such, a diagnosis of Parkinson’s disease is a clinical one; it is only considered definitive after an autopsy. Parkinson’s Disease: A Heterogeneous Disorder What is becoming more evident is that Parkinson’s disease (PD) is a heterogeneous disorder. This has led to proposals to divide PD into two sub- types: 1) Tremor-dependent PD and 2) Postural Instability and Gait Difficulty PD. Parkinson’s disease is seen more frequently in men. There appears to be forms of PD with a genetic basis. Parkinson’s disease is also associated with several comorbidities such as testosterone deficiency or lower bone density. The Movement Disorder Society (MDS) defines Parkinson’s disease as a combined syndrome consisting of “A motor clinical syndrome, with levodopa- responsive parkinsonism, typical clinical characteristics, and an absence of markers suggestive of other disease” and “Pathologic confirmation of α- synuclein (α-Syn) deposition and dopamine neuronal loss in the substantia 1 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com nigra pars compacta (SNpc). Only at this point is the diagnosis termed “definite.” If typical synuclein pathology is not found, the clinical diagnosis is considered incorrect. Likewise, the pathology is “incidental” in the absence of clinical symptoms or attributed to another disease if parkinsonism did not dominate the clinical picture...”1 Parkinson’s disease is slightly more predominant in men, though this increases with age. In individuals aged 50 - 59, the prevalence per 100,000 individuals is 41 in females and 134 in males.1 A recent systematic review and meta-analysis was published synthesizing 47 studies from 1985 to 2010. The studies were geographically diverse, covering North and South America, Asia, Europe and Africa. The prevalence of PD per 100,000 people in general was shown to increase with age: • 41 (95% CI 20-81) for individuals aged 40-49 years • 107 (95% CI 54-211) for individuals aged 50-59 years • 173 (95% CI 88-340) for individuals aged 55-64 years • 428 (95% CI 235-780) for individuals aged 60-69 years • 425 (95% CI 193-939) for individuals aged 65-74 years • 1,087 (95% CI 627-1,883) for individuals aged 70-79 years • 1,903 (95% CI 1,132-3,198) for individuals aged more than 80 years There was some geographic difference noted in the review. For individuals between the ages of 70 and 79, prevalence in Asian patients was less than half of those individuals from Europe, North America and Australia and less than a third of those from South America.2 Gender prevalence of PD (males versus females per 100,000) was shown to vary with age: • 36 vs. 45 for individuals aged 40-49 years • 134 vs. 41 for individuals aged 50-59 years • 233 vs. 150 for individuals aged 55-64 years 2 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com • 389 vs. 392 for individuals aged 60-69 years • 706 vs. 610 for individuals aged 65-74 years • 932 vs. 813 for individuals aged 70-79 years • 2,101 vs. 1,517 for individuals aged more than 80 years Genetics There appears to be forms of PD with a genetic predisposition, with both autosomal dominant and autosomal recessive inheritance. Overall, approximately 15% of cases have a family history of PD. The genes that have been identified to date as being linked to PD include LRRK2, PARK7, PINK1, PRKN, and SNCA genes.1 In mutations of either the LRRK2 or the SNCA gene, inheritance is in an autosomal dominant pattern while in mutations of the PARK7, PINK1 or the PRKN gene, inheritance is in an autosomal recessive pattern. The LRRK2 gene (DRDN), found on chromosome 12, codes for dardarin, a protein Oxidative stress results from the reaction of reactive with both kinase and GRPase activity. Over radicals such as reactive oxygen or nitrogen species 100 different, single amino acid mutations (ROS/RNS) on DNA and cellular proteins that results are known in families with late-onset PD. In in cell damage or death. Basque populations, the most common mutations replace arginine with glycine at position 1441 (Arg1441Gly). In North African Arabs and those of Ashkenazi Jewish background, the most common mutation replaces glycine with serine at position 2019 (Gly2019Ser). In Chinese and Japanese populations, the most common mutation replaces glycine with arginine at position 2385 (Gly2385Arg).1 3 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com The PARK7 gene (Parkinson7, DJ-1), found on chromosome 1, codes for the DJ-1 protein. The precise function of the DJ-1 is not known, though it appears to protect against oxidative stress. DJ-1 could also function as a molecular chaperone. Chaperone molecules play a part in the folding of newly produced proteins and the delivery of damaged proteins to proteasomes for proteolysis. Over 25 different mutations located on the PARK7 gene have been associated with PD. The mutations in PARK7 have been associated with the early-onset form of PD. It is unknown if the altered chaperone function of the DJ-1 protein resulting from these mutations is causally related to PD or if another unknown function is more critical to the etiology of PD.1 The PINK1 gene (PTEN-Induced Putative Kinase 1, PARK6), found on chromosome 1, codes for the PTEN-induced putative kinase1 protein. PTEN- 1 is found at highest levels in the heart and the testes and is found within mitochondria. It appears to protect the mitochondria during periods of high energy demands. Over 70 different mutations inPTEN-1 have been seen in patients with PD, often removing the kinase functionality of the protein.1 The PRKN gene (parkin RBR E3 ubiquitin protein ligase, AR-JP, PARK2), found on chromosome 6, codes for a protein, parkin, which tags damaged, nonfunctional or excess proteins with ubiquitin. Ubiquitin acts as a flag for movement into proteasomes and eventual proteolysis. Parkin may also be involved in the destruction of damaged or otherwise non-functional mitochondria. In addition, parkin may function as a tumor suppressor protein and regulate the production and release of neurotransmitters.1 Over 200 mutations of the PRKN gene have been associated with PD, more commonly with early-onset PD but also with late-onset PD.1 4 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com The GBA gene (glucocerebrosidase) encodes for a lysosomal enzyme associated with PD and may be involved in the clearance of α-synuclein aggregates which play a role in the formation of Lewy bodies. GBA deficiency is also associated with Gaucher’s disease. Individuals with a GBA-associated parkinsonism tend to show symptoms at a younger age and a higher frequency of cognitive changes.1 In Ashkenazi Jews with PD, 15% carried a GBA mutation in one study. In another study, 31.3% of PD patients of Ashkenazi background carried a GBA mutation.2 Most cases of PD, however, appear to be the result of a complex interaction of genetic, medical history and environmental factors, though a recent large- scale meta-analysis of genome-wide association data has identified an additional 28 loci associated with PD.2 Risk Factors There are a number of potential risk factors that have been associated with PD. Increasing age remains the most significant risk factor but the disorder is also consistently associated with pesticide exposure, a history of head trauma that includes an episode of unconsciousness, family history of PD, poliomyelitis, or melanoma, elevated total serum cholesterol levels, higher intake of dairy products (in men), higher levels of serum IL-6, olfactory impairment and trichloroethylene exposure.2-5 Parkinson’s disease is also associated with a family history of melanoma (1st degree relatives). No association of PD has been seen with a family history of colorectal, lung, prostate or breast cancer. In fact, a recent large national record-linkage study found that PD is associated with a decreased risk of cancer with an increased risk of melanoma and breast cancer.2 5 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Conversely, it is less likely that risk factors for PD include mild traumatic brain injury (TBI), smoking or tobacco use, caffeine consumption, alcohol consumption, or a diet high in unsaturated fats. In fact, many of these are inversely related to the risk of PD.14-16 Parkinson’s disease is also associated with several comorbidities including testosterone deficiency, elevated total cholesterol, lower bone density, increased risk of falls, Vitamin D deficiency and anxiety disorders.2 In one prospective cohort study looking at 24,773 Finnish men and 26,153 Finnish women, with 321 of the men and 304 of the women developing PD, total cholesterol greater than 270mg/dL had a hazard ratio of 1.86. However, elevated cholesterol levels after the age of 55 did not appear to be correlated with PD.2 On the other hand, a more recent prospective study examining the effects of statin use on the
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