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Parkinson Disease: HELP
Articles by Daniel D. Truong
Based on 14 articles published since 2010
(Why 14 articles?)
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Between 2010 and 2020, Danny Truong wrote the following 14 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Editorial Editorial and introduction: Behavioral aspects of Parkinson's disease. 2017

Friedman, Joseph H / Bhidayasiri, Roongroj / Truong, Daniel D. ·Butler Hospital, Department of Neurology, Alpert Medical School of Brown University, RI, USA. · Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok 10330, Thailand; Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. · Truong Neuroscience Institute, Parkinson's and Movement Disorders Institute, Orange Coast Memorial Medical Center, Fountain Valley, CA, USA. ·J Neurol Sci · Pubmed #28087061.

ABSTRACT: -- No abstract --

2 Review Diffuse Lewy body disease. 2019

Lin, Yu Wei / Truong, Daniel. ·Taiwan Adventist Hospital, Taipei, Taiwan. · The Truong Neuroscience Institute, Orange Coast Memorial Medical Center, Fountain Valley, CA, USA; Departments of Psychiatry and Neuroscience, UC Riverside, Riverside, CA, USA. Electronic address: dtruong@pmdi.org. ·J Neurol Sci · Pubmed #30807982.

ABSTRACT: Diffuse Lewy body disease, also called dementia with Lewy bodies (DLB), is defined as progressive dementia and pathological Lewy bodies distributed in the central and autonomic nervous systems. The clinical features are dementia, cognitive fluctuations, visual hallucinations, parkinsonism, and REM sleep behavior disorder (RBD). Confirmatory techniques include dopamine transporter imaging, meta-iodobenzylguanidine (MIBG) myocardial scintigraphy, and polysomnography. The pathology finding in DLB is misfolded alpha-synuclein, the main component of Lewy bodies, propagating in the central nervous system. This may interrupt the acetylcholine pathway and activate an inflammatory response. Mutations of several genes have been found in patients with DLB, including SNCA, GBA, and APOE. The differential diagnosis of DLB and Parkinson's disease with dementia (PDD) is a debated issue. Clinical features distinguishing DLB from PDD include the timing of dementia and visual hallucinations, responses to dopaminergic agents and anti-psychotics, and imaging findings. As to the management of DLB, cholinesterase inhibitors are the Level-A recommendation for treating dementia in DLB patients and also are beneficial for treating visual hallucinations and psychotic symptoms. Dopamine agonists have the risk of inducing psychotic symptoms, while levodopa should be used carefully for motor symptoms. Melatonin and clonazepam are effective in controlling RBD. Several other treatment methods are undergoing trials, including pimavanserine, nilotinib, psychological interventions, and behavior therapy.

3 Review Levodopa-induced dyskinesia: clinical features, incidence, and risk factors. 2018

Tran, Tai N / Vo, Trang N N / Frei, Karen / Truong, Daniel D. ·Neurology Department, University Medical Center, Ho Chi Minh City, Vietnam. · Neurology Department, International Neurosurgery Hospital, Ho Chi Minh City, Vietnam. · Loma Linda University, Loma Linda, CA, 92354, USA. · The Truong Neuroscience Institute, Orange Coast Memorial Medical Center, Fountain Valley, CA, 92708, USA. dtruong@pmdi.org. · Department of Psychiatry and Neuroscience, UC Riverside, Riverside, CA, USA. dtruong@pmdi.org. ·J Neural Transm (Vienna) · Pubmed #29971495.

ABSTRACT: Symptoms of Parkinson's disease have been controlled with levodopa for many years; however, motor complications consisting of wearing off of medication effect and dyskinesias tend to occur within a few years of starting levodopa. Motor complications can begin a few months after taking levodopa, with the average time to onset estimated to be 6.5 years. Dyskinesias can be troublesome and require intervention. Levodopa-induced dyskinesia can be composed of a variety of movement disorders including chorea, dystonia, ballism, myoclonus, and akathisia. Based on the clinical pattern, the most common dyskinesia is chorea and choreoathetosis. The clinical manifestations can be divided into three main categories based on their clinical movement patterns and the temporal correlation between the occurrence of dyskinesia and the levodopa dosing: on or peak-dose dyskinesias, biphasic dyskinesias, and Off dyskinesias. Severe cases of dyskinesia have been reported, with the extreme being dyskinesia-hyperpyrexia syndrome. The prevalence of LID has been reported in many studies, but the reported incidence varies. The rate of LID development is from 3 to 94%. The prevalence of LID mainly depends on age at onset, disease duration, and severity, and duration of levodopa therapy. Some of the risk factors for the development of dyskinesia are modifiable. Modifiable risk factors include levodopa dose and body weight. Non-modifiable risk factors include age, gender, duration of disease, clinical subtype, disease progression, disease severity, and genetic factors.

4 Review The sleeping brain in Parkinson's disease: A focus on REM sleep behaviour disorder and related parasomnias for practicing neurologists. 2017

Bhidayasiri, Roongroj / Sringean, Jirada / Rattanachaisit, Watchara / Truong, Daniel D. ·Chulalongkorn Centre of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital and Thai Red Cross Society, Bangkok, Thailand; Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. · Chulalongkorn Centre of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital and Thai Red Cross Society, Bangkok, Thailand. · Parkinson's and Movement Disorders Institute, Fountain Valley, CA, USA. ·J Neurol Sci · Pubmed #28126342.

ABSTRACT: Sleep disorders are identified as common non-motor symptoms of Parkinson's disease (PD) and recently this recognition has been expanded to include parasomnias, encompassing not only REM sleep behaviour disorder (RBD), but also other non-REM forms. RBD, a prototypical parasomnia in PD, exists even in the prodromal stage of the disease, and is characterized by the presence of dream enactment behaviours occurring alongside a loss of normal skeletal muscle atonia during REM sleep. In contrast, non-REM parasomnias are more frequently observed in the late stage PD. However, the development of these disorders often overlaps and it is not uncommon for PD patients to meet the criteria for more than one type of parasomnias, thus making a clinical distinction challenging for practicing neurologists who are not sleep specialists. Indeed, clinical recognition of the predominant form of parasomnia does not just depend on video-polysomnography, but also on an individual physician's clinical acumen in delineating pertinent clinical history to determine the most likely diagnosis and proceed accordingly. In this review article, we highlight the various forms of parasomnias that have been reported in PD, including, but not limited to, RBD, with a focus on clinical symptomatology and implications for clinical practice. In addition, we review the differences in PD-related parasomnias compared to those seen in general populations. With advances in sleep research and better technology for ambulatory home monitoring, it is likely that many unanswered questions on PD-related parasomnias will soon be resolved resulting in better management of this nocturnal challenge in PD.

5 Review Hallucinations and the spectrum of psychosis in Parkinson's disease. 2017

Frei, Karen / Truong, Daniel D. ·Loma Linda University, Loma Linda, CA, United States. Electronic address: drkpfrei@gmail.com. · The Parkinson's and Movement Disorders Institute, Fountain Valley, CA, United States. ·J Neurol Sci · Pubmed #28108020.

ABSTRACT: Hallucinations and psychosis can be a part of Parkinson's disease and are considered to be a nonmotor symptom or a neuropsychiatric complication of the disease. Hallucinations of different modalities and delusions can occur beyond the common visual hallucinations. The various types of hallucinations and psychotic symptoms comprising the spectrum of Parkinson's disease psychosis is the subject of this review article.

6 Review Therapeutic strategies for nonmotor symptoms in early Parkinson's disease: the case for a higher priority and stronger evidence. 2012

Bhidayasiri, Roongroj / Truong, Daniel D. ·Chulalongkorn Center of Excellence on Parkinson's Disease and Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, 10330, Thailand. rbh1@ucla.edu ·Parkinsonism Relat Disord · Pubmed #22166405.

ABSTRACT: It is now recognized that the neuropathology of early Parkinson's disease (PD) is not limited to the nigrostriatal dopaminergic system, but also involves various brainstem nuclei, the hypothalamus, the olfactory system, and the peripheral autonomic nervous system. Given the disseminated neuropathology of early PD, the earliest clinical signs include a myriad of non-motor manifestations including sleep-wake cycle regulation, cognition, mood and motivation, olfactory and gustatory functions, autonomic functions, and sensory and pain processing. Despite this realization, there is clearly a paucity of trials that have systematically evaluated the treatment of non-motor symptoms of PD in the early stages. For example, only one large-scale, placebo-controlled randomized trial has been conducted on the treatment of depression in PD patients. There are no reports of randomized controlled trials of therapeutic agents looking at the frequently reported anxiety and fatigue in early PD patients. Based on this lack of evidence, therapy for early non-motor manifestations is often ignored and the focus remains on dopamine replacement strategies with main outcomes being restricted to motor measurements, such as the Unified Parkinson's Disease Rating Scale. This article presents the case for prioritizing well-designed, controlled clinical trials of therapeutic interventions focusing on non-motor symptoms in early PD patients.

7 Clinical Trial Pooled Analyses of Phase III Studies of ADS-5102 (Amantadine) Extended-Release Capsules for Dyskinesia in Parkinson's Disease. 2018

Elmer, Lawrence W / Juncos, Jorge L / Singer, Carlos / Truong, Daniel D / Criswell, Susan R / Parashos, Sotirios / Felt, Larissa / Johnson, Reed / Patni, Rajiv. ·Department of Neurology, University of Toledo College of Medicine, 3120 Glendale Avenue, Toledo, OH, 43614, USA. Lawrence.Elmer@utoledo.edu. · Department of Neurology and Movement Disorders, Emory University School of Medicine, Atlanta, GA, USA. · Department of Neurology, University of Miami, Miami, FL, USA. · The Parkinson's and Movement Disorder Institute, Fountain Valley, CA, USA. · Department of Neurology, Washington University, St. Louis, MO, USA. · Struthers Parkinson's Center, Golden Valley, MN, USA. · Adamas Pharmaceuticals, Inc., Emeryville, CA, USA. ·CNS Drugs · Pubmed #29532440.

ABSTRACT: BACKGROUND: Although levodopa is considered the most effective pharmacotherapy for motor symptoms of Parkinson's disease (PD), chronic use is associated with motor complications, including fluctuating response and unpredictable, involuntary movements called dyskinesia. ADS-5102 (amantadine) extended-release (ER) capsules (GOCOVRI OBJECTIVE: In this study, we present pooled results from two randomized, double-blind, placebo-controlled, phase III ADS-5102 trials. PATIENTS AND METHODS: The two studies in PD patients with dyskinesia shared design and eligibility criteria, differing only in treatment duration. Results from common assessment time points were pooled. RESULTS: At 12 weeks, the least squares (LS) mean change in total score on the Unified Dyskinesia Rating Scale among 100 patients randomized to ADS-5102 and 96 patients randomized to placebo was - 17.7 (standard error [SE] 1.3) vs. - 7.6 (1.3) points, respectively (- 10.1 points, 95% confidence interval [CI] - 13.8, - 6.5; p < 0.0001). The relative treatment difference between groups was 27.3% (p < 0.0001). At 12 weeks, the LS mean change in OFF time was - 0.59 (0.21) vs. +0.41 (0.20) h/day, a difference of - 1.00 h/day (95% CI - 1.57, - 0.44; p = 0.0006). For both efficacy measures, a significant difference from placebo was attained by two weeks, the first post-baseline assessment, and was maintained throughout 12 weeks. In the pooled ADS-5102 group, the most common adverse events were hallucination, dizziness, dry mouth, peripheral edema, constipation, falls, and orthostatic hypotension. CONCLUSIONS: These analyses provide further evidence supporting ADS-5102 as an adjunct to levodopa for treating both dyskinesia and OFF time in PD patients with dyskinesia. Clinicaltrials.gov identifier: NCT02136914 and NCT02274766.

8 Clinical Trial ADS-5102 (Amantadine) Extended-Release Capsules for Levodopa-Induced Dyskinesia in Parkinson Disease (EASE LID Study): A Randomized Clinical Trial. 2017

Pahwa, Rajesh / Tanner, Caroline M / Hauser, Robert A / Isaacson, Stuart H / Nausieda, Paul A / Truong, Daniel D / Agarwal, Pinky / Hull, Keith L / Lyons, Kelly E / Johnson, Reed / Stempien, Mary Jean. ·Department of Neurology, University of Kansas Medical Center, Kansas City. · Department of Neurology, University California-San Francisco. · Parkinson's Disease Research, Education and Clinic Center, San Francisco Veterans Affairs Medical Center, San Francisco, California. · Health Byrd Parkinson's Disease and Movement Disorders Center of Excellence, University of South Florida, Tampa. · Parkinson's Disease and Movement Disorders Center of Boca Raton, Boca Raton, Florida. · Wisconsin Institute for Neurologic and Sleep Disorders, Milwaukee. · The Parkinson's and Movement Disorder Institute, Fountain Valley, California. · Booth Gardner Parkinson's Care Center, Evergreen Health, Kirkland, Washington. · Raleigh Neurology Associates, Raleigh, North Carolina. · Adamas Pharmaceuticals Inc, Emeryville, California. ·JAMA Neurol · Pubmed #28604926.

ABSTRACT: Importance: Medical treatment of levodopa-induced dyskinesia (LID) in Parkinson disease (PD) is an unmet need. Objective: To evaluate the efficacy and safety of ADS-5102 (amantadine) extended-release 274-mg capsules for treatment of LID in patients with PD. Design, Setting, and Participants: A randomized, double-blind, placebo-controlled clinical trial was conducted between May 7, 2014, and July 22, 2015, at 44 North American sites among patients with PD treated with levodopa who experienced at least 1 hour of troublesome dyskinesia per day with at least mild functional impact. Interventions: Patients were randomized to receive placebo or 274 mg of ADS-5102 administered orally at bedtime for up to 25 weeks. Main Outcomes and Measures: The primary efficacy analysis was the change from baseline to week 12 in the Unified Dyskinesia Rating Scale total score for ADS-5102 vs placebo in the modified intent-to-treat population. OFF time (amount of time the PD medication is not controlling motor symptoms) was a key secondary end point. Safety analyses included all patients who received the study drug (ADS-5102 or placebo). Results: A total of 189 patients were screened, and 126 were randomized; the modified intent-to-treat population included 121 patients (51 women and 70 men; mean [SD] age, 64.7 [9.1] years). At week 12, the least-squares mean (SE) change in the Unified Dyskinesia Rating Scale score was -15.9 (1.6) for ADS-5102 (n = 63) and -8.0 (1.6) for placebo (n = 58) (treatment difference, -7.9; 95% CI, -12.5 to -3.3; P < .001). OFF time decreased by a mean (SE) of 0.6 (0.3) hours for ADS-5102 and increased by 0.3 (0.3) hours for placebo (treatment difference, -0.9 hours; 95% CI, -1.6 to -0.2; P = .02). Common adverse events for ADS-5102 vs placebo included visual hallucinations (15 [23.8%] vs 1 [1.7%]), peripheral edema (15 [23.8%] vs 0), and dizziness (14 [22.2%] vs 0). Adverse events led to treatment discontinuation for 13 patients receiving ADS-5102 (20.6%) vs 4 patients receiving placebo (6.9%). Conclusions and Relevance: ADS-5102, 274 mg at bedtime, may be an effective treatment for LID. An additional benefit is reduced OFF time. To our knowledge, this is the first demonstration of an oral treatment reducing both LID and OFF time in patients with PD with dyskinesia. Trial Registration: clinicaltrials.gov Identifier: NCT02136914.

9 Clinical Trial Caffeine and Progression of Parkinson Disease: A Deleterious Interaction With Creatine. 2015

Simon, David K / Wu, Cai / Tilley, Barbara C / Wills, Anne-Marie / Aminoff, Michael J / Bainbridge, Jacquelyn / Hauser, Robert A / Schneider, Jay S / Sharma, Saloni / Singer, Carlos / Tanner, Caroline M / Truong, Daniel / Wong, Pei Shieen. ·*Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; †Department of Biostatistics, School of Public Health, University of Texas Health Science Center at Houston, Houston, TX; ‡Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA; §Department of Neurology, University of California, San Francisco, CA; ∥Department of Clinical Pharmacy and Neurology, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado, Aurora, CO; ¶Department of Neurology, University of South Florida, Tampa, FL; #Department of Pathology, Anatomy and Cell Biology, Parkinson's Disease Research Unit, Thomas Jefferson University, Philadelphia, PA; **Clinical Trials Coordination Center, University of Rochester Medical Center, Rochester, NY; ††Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL; ‡‡Parkinson's Disease Research Education and Clinical Center, San Francisco Veteran's Affairs Medical Center, San Francisco, CA; §§The Parkinson's and Movement Disorder Institute, Fountain Valley, CA; and ∥∥Singapore General Hospital, Singapore. ·Clin Neuropharmacol · Pubmed #26366971.

ABSTRACT: OBJECTIVE: Increased caffeine intake is associated with a lower risk of Parkinson disease (PD) and is neuroprotective in mouse models of PD. However, in a previous study, an exploratory analysis suggested that, in patients taking creatine, caffeine intake was associated with a faster rate of progression. In the current study, we investigated the association of caffeine with the rate of progression of PD and the interaction of this association with creatine intake. METHODS: Data were analyzed from a large phase 3 placebo-controlled clinical study of creatine as a potentially disease-modifying agent in PD. Subjects were recruited for this study from 45 movement disorders centers across the United States and Canada. A total of 1741 subjects with PD participated in the primary clinical study, and caffeine intake data were available for 1549 of these subjects. The association of caffeine intake with rate of progression of PD as measured by the change in the total Unified Parkinson Disease Rating Scale score and the interaction of this association with creatine intake were assessed. RESULTS: Caffeine intake was not associated with the rate of progression of PD in the main analysis, but higher caffeine intake was associated with significantly faster progression among subjects taking creatine. CONCLUSIONS: This is the largest and longest study conducted to date that addresses the association of caffeine with the rate of progression of PD. These data indicate a potentially deleterious interaction between caffeine and creatine with respect to the rate of progression of PD.

10 Article Effect of using a wearable device on clinical decision-making and motor symptoms in patients with Parkinson's disease starting transdermal rotigotine patch: A pilot study. 2019

Isaacson, Stuart H / Boroojerdi, Babak / Waln, Olga / McGraw, Martha / Kreitzman, David L / Klos, Kevin / Revilla, Fredy J / Heldman, Dustin / Phillips, Maureen / Terricabras, Dolors / Markowitz, Michael / Woltering, Franz / Carson, Stan / Truong, Daniel. ·Parkinson's Disease and Movement Disorder Center of Boca Raton, Boca Raton, FL, USA. Electronic address: isaacson@ParkinsonsCenter.org. · UCB Pharma, Monheim am Rhein, Germany. Electronic address: babak.boroojerdi@ucb.com. · Houston Methodist Neurological Institute, Houston, TX, USA. Electronic address: owaln@houstonmethodist.org. · Central Dupage Hospital/Northwestern Medicine, Winfield, IL, USA. Electronic address: martha.mcgraw@nm.org. · Parkinson's Disease and Movement Disorders Center of Long Island, Commack, NY, USA. Electronic address: ParkinsonsCenterLI@gmail.com. · Movement Disorder Clinic of Oklahoma, Tulsa, OK, USA. Electronic address: kevin.klos@mdcok.com. · Greenville Health System, Greenville, SC, USA; Division of Neurology, University of South Carolina School of Medicine Greenville, Greenville, SC, USA. Electronic address: frevilla@ghs.org. · Great Lakes NeuroTechnologies, Cleveland, OH, USA. Electronic address: dheldman@glneurotech.com. · Great Lakes NeuroTechnologies, Cleveland, OH, USA. Electronic address: maureen.phillips@intel.com. · UCB Pharma, Slough, UK. Electronic address: terricabras.dolors@gmail.com. · UCB Pharma, Raleigh, NC, USA. Electronic address: michael.markowitz@ucb.com. · UCB Pharma, Monheim am Rhein, Germany. Electronic address: franz.woltering@ucb.com. · UCB Pharma, Raleigh, NC, USA. Electronic address: stan.carson@ucb.com. · Parkinson's and Movement Disorder Institute, Fountain Valley, CA, USA. Electronic address: dtruong@pmdi.org. ·Parkinsonism Relat Disord · Pubmed #30948242.

ABSTRACT: BACKGROUND: Feedback from wearable biosensors may help assess motor function in Parkinson's disease (PD) patients and titrate medication. Kinesia 360 continuously monitors motor symptoms via wrist and ankle sensors. METHODS: PD0049 was a 12-week pilot study to investigate whether using Kinesia 360 at home could improve motor symptom management in PD patients starting transdermal dopamine agonist rotigotine. Adults with PD and insufficiently controlled motor symptoms (prescribed rotigotine) were randomized 1:1 to Control Group (CG) or Experimental Group (EG) before starting rotigotine. Motor symptoms were assessed in all patients at baseline and Week 12 (W12) using Unified PD Rating Scale (UPDRS) III and Kinesia ONE, which measures standardized motor tasks via a sensor on the index finger. Between baseline and W12, EG used Kinesia 360 at home; clinicians used the data to supplement standard care in adjusting rotigotine dosage. RESULTS: At W12, least squares mean improvements in UPDRS II (-2.1 vs 0.5, p = 0.004) and UPDRS III (-5.3 vs -1.0, p = 0.134) were clinically meaningfully greater, and mean rotigotine dosage higher (4.8 vs 3.9 mg/24 h) in EG (n = 19) vs CG (n = 20). Mean rotigotine dosage increase (+2.8 vs + 1.9 mg/24 h) and mean number of dosage changes (2.8 vs 1.8) during the study were higher in EG vs CG. Tolerability and retention rates were similar. CONCLUSION: Continuous, objective, motor symptom monitoring using a wearable biosensor as an adjunct to standard care may enhance clinical decision-making, and may improve outcomes in PD patients starting rotigotine.

11 Article Caffeine, creatine, GRIN2A and Parkinson's disease progression. 2017

Simon, David K / Wu, Cai / Tilley, Barbara C / Lohmann, Katja / Klein, Christine / Payami, Haydeh / Wills, Anne-Marie / Aminoff, Michael J / Bainbridge, Jacquelyn / Dewey, Richard / Hauser, Robert A / Schaake, Susen / Schneider, Jay S / Sharma, Saloni / Singer, Carlos / Tanner, Caroline M / Truong, Daniel / Wei, Peng / Wong, Pei Shieen / Yang, Tianzhong. ·Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. Electronic address: dsimon1@bidmc.harvard.edu. · Department of Biostatistics, University of Texas Health Science Center School of Public Health at Houston, Houston, TX 77030, USA. Electronic address: Cai.Wu@uth.tmc.edu. · Department of Biostatistics, University of Texas Health Science Center School of Public Health at Houston, Houston, TX 77030, USA. Electronic address: Barbara.C.Tilley@uth.tmc.edu. · Institute of Neurogenetics, University of Luebeck, 23538 Luebeck, Germany. Electronic address: katja.lohmann@neuro.uni-luebeck.de. · Institute of Neurogenetics, University of Luebeck, 23538 Luebeck, Germany. Electronic address: christine.klein@neuro.uni-luebeck.de. · Department of Neurology, University of Alabama at Birmingham, Birmingham, AL 35233, USA; Center for Genomic Medicine, HudsonAlpha Institute for Biotechnology, Huntsville, AL 35806, USA. Electronic address: haydehpayami@uabmc.edu. · Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: AWILLS@mgh.harvard.edu. · Department of Neurology, University of California, San Francisco, USA. Electronic address: Michael.Aminoff@ucsf.edu. · University of Colorado, Anschutz Medical Campus, Skaggs School of Pharmacy and Pharmaceutical Sciences, Department of Clinical Pharmacy and Neurology, Aurora, CO, USA. Electronic address: Jacci.Bainbridge@ucdenver.edu. · University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: richard.dewey@utsouthwestern.edu. · Department of Neurology, University of South Florida, Tampa, FL, USA. Electronic address: rhauser@health.usf.edu. · Institute of Neurogenetics, University of Luebeck, 23538 Luebeck, Germany. Electronic address: susen.schaake@neuro.uni-luebeck.de. · Department of Pathology, Anatomy and Cell Biology, Parkinson's Disease Research Unit, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address: Jay.Schneider@jefferson.edu. · Clinical Trials Coordination Center, University of Rochester Medical Center, Rochester, NY 14642, USA. Electronic address: saloni.sharma@chet.rochester.edu. · Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address: csinger@med.miami.edu. · Parkinson's Disease Research Education and Clinical Center, San Francisco Veteran's Affairs Medical Center, Department of Neurology, University of California, San Francisco, CA, USA. Electronic address: Caroline.Tanner@ucsf.edu. · The Parkinson's and Movement Disorder Institute, Fountain Valley, CA, USA. Electronic address: dtruong@pmdi.org. · Department of Biostatistics, University of Texas Health Science Center School of Public Health at Houston, Houston, TX 77030, USA. Electronic address: Peng.Wei@uth.tmc.edu. · University of Colorado, Anschutz Medical Campus, Skaggs School of Pharmacy and Pharmaceutical Sciences, Department of Clinical Pharmacy and Neurology, Aurora, CO, USA; Singapore General Hospital, Singapore 169608, Singapore. Electronic address: pei.wong@ucdenver.edu. · Department of Biostatistics, University of Texas Health Science Center School of Public Health at Houston, Houston, TX 77030, USA. Electronic address: Tianzhong.Yang@uth.tmc.edu. ·J Neurol Sci · Pubmed #28320167.

ABSTRACT: Caffeine is neuroprotective in animal models of Parkinson's disease (PD) and caffeine intake is inversely associated with the risk of PD. This association may be influenced by the genotype of GRIN2A, which encodes an NMDA-glutamate-receptor subunit. In two placebo-controlled studies, we detected no association of caffeine intake with the rate of clinical progression of PD, except among subjects taking creatine, for whom higher caffeine intake was associated with more rapid progression. We now have analyzed data from 420 subjects for whom DNA samples and caffeine intake data were available from a placebo-controlled study of creatine in PD. The GRIN2A genotype was not associated with the rate of clinical progression of PD in the placebo group. However, there was a 4-way interaction between GRIN2A genotype, caffeine, creatine and the time since baseline. Among subjects in the creatine group with high levels of caffeine intake, but not among those with low caffeine intake, the GRIN2A T allele was associated with more rapid progression (p=0.03). These data indicate that the deleterious interaction between caffeine and creatine with respect to rate of progression of PD is influenced by GRIN2A genotype. This example of a genetic factor interacting with environmental factors illustrates the complexity of gene-environment interactions in the progression of PD.

12 Article Impact of Depression on Progression of Impairment and Disability in Early Parkinson's Disease. 2015

Bega, Danny / Luo, Sheng / Fernandez, Hubert / Chou, Kelvin / Aminoff, Michael / Parashos, Sotirios / Walker, Harrison / Russell, David S / Christine, Chadwick W / Dhall, Rohit / Singer, Carlos / Bodis-Wollner, Ivan / Hamill, Robert / Truong, Daniel / Mari, Zoltan / Glazmann, Sofya / Huang, Meilin / Houston, Emily / Simuni, Tanya. ·Northwestern University, Chicago, Illinois, USA. · University of Texas Health Science Center, Houston, Texas, USA. · Cleveland Clinic, Cleveland, Ohio, USA. · University of Michigan, Ann Arbor, Michigan, USA. · University of California San Francisco, San Francisco, California, USA. · Minneapolis Clinic, Minneapolis, Minnesota, USA. · University of Alabama at Birmingham, Birmingham, Alabama, USA. · Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA. · Muhammad Ali Parkinson Center, Phoenix, Arizona, USA. · University of Miami, Miami, Florida, USA. · State University of New York, Syracuse, New York, USA. · University of Vermont, Burlington, Vermont, USA. · Parkinson and Movement Disorders Institute, Fountain Valley, California, USA. · Johns Hopkins University, Baltimore, Maryland, USA. ·Mov Disord Clin Pract · Pubmed #28393083.

ABSTRACT: BACKGROUND: Depression is one of the most common nonmotor symptoms associated with Parkinson's disease (PD), yet the impact of depression on progression of disease is unclear. OBJECTIVE: The aim of this study was to prospectively characterize the relationship between depressive symptoms and measures of disease progression in a large sample of patients with early, medically treated PD. METHODS: Baseline and longitudinal Beck Depression Inventory (BDI) scores from participants in the NINDS Exploratory Trials in PD Long Term Study 1 were correlated with changes in multiple measures of disease severity over 5 years. Multivariate analysis of predictors of change in BDI was performed. RESULTS: Of 1,741 participants, 746 completed 5-year assessments and were included. Mean age was 62.00 years (standard deviation [SD]: 9.22) and mean disease duration was 1.69 years (SD, 1.16). Mean BDI score was 6.24 (SD, 5.02) at baseline and 8.57 (SD, 6.60) at 5 years. Baseline BDI score was strongly associated with rate of change in all examined measures of disease severity. In multivariate analysis, BDI 5-year change was associated with change in UPDRS Part I (excluding depression item; CONCLUSIONS: Worse baseline BDI scores are associated with a decline in multiple measures of disease severity in PD. Worsening of BDI at 5 years was associated with worsening in UPDRS Part I and quality-of-life measures, but not with motor or cognitive measures.

13 Article Amantadine extended release for levodopa-induced dyskinesia in Parkinson's disease (EASED Study). 2015

Pahwa, Rajesh / Tanner, Caroline M / Hauser, Robert A / Sethi, Kapil / Isaacson, Stuart / Truong, Daniel / Struck, Lynn / Ruby, April E / McClure, Natalie L / Went, Gregory T / Stempien, Mary Jean. ·University of Kansas Medical Center, Kansas City, Kansas, USA. · The Parkinson's Institute, Sunnyvale, CA, San Francisco Veterans Affairs Medical Center and University of California-San Francisco, San Francisco, California, USA. · University of South Florida, Tampa, Florida, USA. · Georgia Regents University, Augusta, Georgia, USA. · Parkinson's Disease and Movement Disorders Center, Boca Raton, Florida, USA. · Parkinson's & Movement Disorder Institute, Fountain Valley, California, USA. · Iowa Health Physicians, Des Moines, Iowa, USA. · Adamas Pharmaceuticals, Inc., Emeryville, California, USA. ·Mov Disord · Pubmed #25650051.

ABSTRACT: ADS-5102 is a long-acting, extended-release capsule formulation of amantadine HCl administered once daily at bedtime. This study investigated the safety, efficacy, and tolerability of ADS-5102 in Parkinson's disease (PD) patients with levodopa-induced dyskinesia. This was a randomized, double-blind, placebo-controlled, parallel-group study of 83 PD patients with troublesome dyskinesia assigned to placebo or one of three doses of ADS-5102 (260 mg, 340 mg, 420 mg) administered daily at bedtime for 8 weeks. The primary efficacy analysis compared change from baseline to week 8 in Unified Dyskinesia Rating Scale (UDysRS) total score for 340 mg ADS-5102 versus placebo. Secondary outcome measures included change in UDysRS for 260 mg, 420 mg, Fatigue Severity Scale (FSS), Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS), patient diary, Clinician's Global Impression of Change, and Parkinson's Disease Questionnaire (PDQ-39). ADS-5102 340 mg significantly reduced dyskinesia versus placebo (27% reduction in UDysRS, P = 0.005). In addition, ADS-5102 significantly increased ON time without troublesome dyskinesia, as assessed by PD patient diaries, at 260 mg (P = 0.004), 340 mg (P = 0.008) and 420 mg (P = 0.018). Adverse events (AEs) were reported for 82%, 80%, 95%, and 90% of patients in the placebo, 260-mg, 340-mg, and 420-mg groups, respectively. Constipation, hallucinations, dizziness, and dry mouth were the most frequent AEs. Study withdrawal rates were 9%, 15%, 14%, and 40% for the placebo, 260-mg, 340-mg, and 420-mg groups, respectively. All study withdrawals in the active treatment groups were attributable to AEs. ADS-5102 was generally well tolerated and resulted in significant and dose-dependent improvements in dyskinesia in PD patients.

14 Article Circadian dysfunction in a mouse model of Parkinson's disease. 2011

Kudo, Takashi / Loh, Dawn H / Truong, Danny / Wu, Yingfei / Colwell, Christopher S. ·Department of Psychiatry & Biobehavioral Sciences, University of California-Los Angeles, Los Angeles, CA 90024, USA. ·Exp Neurol · Pubmed #21864527.

ABSTRACT: Many Parkinson's disease (PD) patients exhibit sleep disorders as part of their symptoms with evidence suggesting that REM sleep disorders may be intimately associated with this disease. Possible dysfunction in the circadian system in PD has received less attention, yet problems in circadian timing are common in neurodegenerative diseases. In the present study, we examined the expression of daily and circadian rhythms in the alpha-synuclein overexpressing (ASO) transgenic line. We found selective deficits in the expression of circadian rhythms of locomotor activity, including lower night-time activity and greater fragmentation in the wheel-running activity in this PD model. These alterations were prominent in young adult (3-4 mo) ASO mice and worsened progressively with age, consistent with prior reports of age-related loss of motor skills. The temporal distribution of sleep was also altered in the ASO mice compared to littermate controls. In the ASO mice, the peak/trough expression of the clock gene PERIOD2 was normal in the master pacemaker of the circadian system: the suprachiasmatic nucleus (SCN); however, the daytime firing rate of SCN neurons was reduced in the mutant mice. Together, this data raises the possibility that a weakening of circadian output is a core feature of PD. The reduction in magnitude of circadian output would be expected to have functional consequences throughout the body.