Early treatment of Parkinson's disease: opportunities for managed care

982045 Nebraska Medical Center, Omaha, NE 68198-2045. E-mail: dlmurman@
The American journal of managed care (Impact Factor: 2.26). 09/2012; 18(7 Suppl):s183-8.
Source: PubMed


The diagnosis and treatment of Parkinson's disease (PD) typically occur when the disease has already progressed to a relatively advanced stage in which motor symptoms are clearly evident and substantial neurophysiological damage has already taken place. Nonmotor symptoms, which account for a large proportion of PD symptoms, usually emerge much earlier and offer both an early indication for treatment and a therapeutic target. A growing body of data from the medical literature points to several critical advantages that may be associated with early therapeutic intervention in PD. The most evident benefit of early intervention is a reduction in symptoms, particularly dyskinesia, and the delay of levodopa initiation. Clinical trials suggest but have yet to conclusively demonstrate that early treatment can slow disease progression. Both the diminishment of symptoms and the potential for slowing disease progression have large implications for improving patient quality of life. The enormous direct costs associated with PD would also likely be reduced over the long term with earlier treatment. The great majority of costs attributable to PD occur when the disease is at its most advanced stage and when symptoms are most severe. An early-treatment strategy that diminishes symptoms and that has the potential to slow disease progression could have a meaningful impact on PD expenditures. Adherence, too, must be taken into consideration, particularly since PD patients are generally poorly adherent to prescribed therapies, especially therapies with complex dosing schedules. Taking advantage of more convenient and adherencefriendly drug formulations may further help to improve outcomes and lower costs in PD.

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    • "Alternatively, therapy may be achieved by utilizing drugs that are currently used for other diseases that cause symptoms similar to those in the early stage of prion diseases, that may show similar efficacy against prions, or by developing new targeted drugs. Such early intervention may limit brain damage, hence delaying the appearance of clinical symptoms, and perhaps also reducing their severity, thus improving the patient's quality of life and resulting in cost savings (Murman, 2012). This could be possible because the early symptoms of such diseases are usually very mild and common to other diseases because they are likely due to reversible functional disorders, which if not treated promptly, would become definitive due to brain impairment and progressively worsen until dementia (Sheinerman & Umansky, 2013). "
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    ABSTRACT: Development of numerous advanced techniques in recent years have allowed detection of the pathological prion protein (PrPTSE), the unique marker of transmissible spongiform encephalopathies (TSEs, or prion diseases), in the blood of animals and humans; however, an ante-mortem screening test that can be used for the routine diagnosis of human prion diseases remains unavailable. A critical, analytical review of all the diagnostic assays developed to date will allow an evaluation of progress in this field and may facilitate the identification of the possible reason/s for this delay. Thus, in this review, I provide a detailed overview of the techniques currently available for detecting PrPTSE and other markers of the disease in blood, as well as an analysis of the significance, feasibility, reliability, and the application spectrum for these methods. I highlight that factors intrinsic and extrinsic to blood may interfere with the detection of PrPTSE/prions, and that this is not yet taken into account in current tests. This may inspire researchers in this field to not only aspire to increase test sensitivity but also to adopt other strategies in order to identify and overcome the limitations that hamper the development of a successful routine blood test for prion diseases.
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    ABSTRACT: The localization of yellow fluorescent protein (YFP)-tagged HSP70 proteins was employed to identify stress-sensitive sites in human neurons following temperature elevation. Stable lines of human SH-SY5Y neuronal cells were established that expressed YFP-tagged protein products of the human inducible HSP70 genes HSPA6 (HSP70B') and HSPA1A (HSP70-1). Following a brief period of thermal stress, YFP-tagged HSPA6 and HSPA1A rapidly appeared at centrioles in the cytoplasm of human neuronal cells, with HSPA6 demonstrating a more prolonged signal compared to HSPA1A. Each centriole is composed of a distal end and a proximal end, the latter linking the centriole doublet. The YFP-tagged HSP70 proteins targeted the proximal end of centrioles (identified by γ-tubulin marker) rather than the distal end (centrin marker). Centrioles play key roles in cellular polarity and migration during neuronal differentiation. The proximal end of the centriole, which is involved in centriole stabilization, may be stress-sensitive in post-mitotic, differentiating human neurons.
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    ABSTRACT: Purpose The influence of mental illness early in life on the subsequent risk of Parkinson's disease (PD) and its clinical picture remain obscure. This study investigated the effects of psychiatric diseases on a subsequent PD diagnosis. Methods We used the Longitudinal Health Insurance Database 2000 of Taiwan to identify 73 597 patients who visited ambulatory care centers or were hospitalized with a first-time diagnosis of anxiety, affective disorders, or schizophrenia between 2001 and 2003 as the study cohort. We also randomly selected 220 791 enrollees matched with the study cohort for comparison. Each patient was individually tracked for 6 years to identify a subsequent PD diagnosis. Stratified Cox proportional hazard regressions were performed for the analysis. Results The incidence rate of PD per 1000 person-years was 4.91 (95% confidence interval [CI)] 4.71–5.12) and 1.63 (95% CI: 1.56–1.70) for the psychiatric and comparison groups, respectively. Patients with psychiatric illnesses were more vulnerable to developing PD than nonpsychiatric individuals, exhibiting a 2.38-fold increased risk (95% CI: 2.23–2.53) after other covariates were considered. Furthermore, patients with schizophrenia exhibited the highest risk for developing PD. Conclusions We suggest effective monitoring of patients with psychiatric disturbances for potential long-term neurodegenerative diseases.
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