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Kurtgöz A, Genç M. Spiritual Care Perspectives of Elderly Individuals with Parkinson's Disease and Formal Caregivers: A Qualitative Study in Turkish Nursing Homes. JOURNAL OF RELIGION AND HEALTH 2024; 63:2106-2124. [PMID: 38042960 DOI: 10.1007/s10943-023-01963-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Accepted: 11/13/2023] [Indexed: 12/04/2023]
Abstract
This study aimed to determine the perceptions and experiences of elderly individuals with Parkinson's disease and formal caregivers regarding spiritual care. A qualitative study was conducted using a descriptive phenomenological design. Fifteen formal caregivers and eight elderly individuals with Parkinson's disease from two nursing homes in Türkiye participated in the study. Data were collected through face-to-face individual interviews, and thematic analysis was employed to examine the data. Two themes were obtained from the data analysis: (I) spiritual care in nursing homes and (II) living with Parkinson's disease in nursing homes. Findings showed that living in a nursing home with Parkinson's disease affects the spiritual dimensions of elderly individuals and increases their spiritual needs. Additionally, it was found that although formal caregivers implemented a diverse range of practices to address the spiritual care needs of individuals residing in a nursing home, they did not offer any specific spiritual care practices for individuals with Parkinson's disease. Based on our findings, it is considered necessary to have spiritual counselors and formal caregivers with expertise in Parkinson's disease in nursing homes.
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Affiliation(s)
- Aslı Kurtgöz
- Department of Therapy and Rehabilitation, Sabuncuoglu Serefeddin Health Services Vocational School, Amasya University, Amasya, 05100, Türkiye.
| | - Mehtap Genç
- Department of Nursing, Health Science Faculty, Karamanoğlu Mehmetbey University, Karaman, Türkiye
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Reyes-Pérez P, García-Marín LM, Aman AM, Antar T, Flores-Ocampo V, Mitchell BL, Medina-Rivera A, Rentería ME. Investigating the Shared Genetic Etiology Between Parkinson's Disease and Depression. JOURNAL OF PARKINSON'S DISEASE 2024; 14:483-493. [PMID: 38457145 PMCID: PMC11091633 DOI: 10.3233/jpd-230176] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Accepted: 01/11/2024] [Indexed: 03/09/2024]
Abstract
Background Depression is a common symptom in Parkinson's disease (PD), resulting from underlying neuropathological processes and psychological factors. However, the extent to which shared genetic risk factors contribute to the relationship between depression and PD is poorly understood. Objective To examine the effects of common genetic variants influencing the etiology of PD and depression risk at the genome-wide and local genomic regional level. Methods We comprehensively investigated the genetic relationship between PD and depression using genome-wide association studies data. First, we estimated the genetic correlation at the genome-wide level using linkage-disequilibrium score regression, followed by local genetic correlation analysis using the GWAS-pairwise method and functional annotation to identify genes that may jointly influence the risk for both traits. Also, we performed Latent Causal Variable, Latent Heritable Confounder Mendelian Randomization, and traditional Mendelian Randomization analyses to investigate the potential causal relationship. Results Although the genetic correlation between PD and depression was not statistically significant at the genome-wide level, GWAS-pairwise analyses identified 16 genomic segments associated with PD and depression, implicating nine genes. Further analyses revealed distinct patterns within individual genes, suggesting an intricate pattern. These genes involve various biological processes, including neurotransmitter regulation, senescence, and nucleo-cytoplasmic transport mechanisms. We did not observe genetic evidence of causality between PD and depression. Conclusions Our findings did not support a genome-wide genetic correlation or a causal association between both conditions. However, we identified genomic segments but identified genomic segments linked to distinct biological pathways influencing their etiology.Further research is needed to understand their functional consequences.
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Affiliation(s)
- Paula Reyes-Pérez
- Laboratorio Internacional de Investigación Sobre el Genoma Humano, Universidad Nacional Autónoma de México, Juriquilla, Querétaro, México
| | - Luis M. García-Marín
- Laboratorio Internacional de Investigación Sobre el Genoma Humano, Universidad Nacional Autónoma de México, Juriquilla, Querétaro, México
- Mental Health and Neuroscience Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia
- School of Biomedical Sciences, Faculty of Medicine, University of Queensland, Brisbane, QLD, Australia
| | - Asma M. Aman
- Mental Health and Neuroscience Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia
- School of Biomedical Sciences, Faculty of Medicine, University of Queensland, Brisbane, QLD, Australia
| | - Tarek Antar
- Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA
| | - Victor Flores-Ocampo
- Laboratorio Internacional de Investigación Sobre el Genoma Humano, Universidad Nacional Autónoma de México, Juriquilla, Querétaro, México
- Licenciatura en Ciencias Genómicas, Escuela Nacional de Estudios Superiores Unidad Juriquilla, Universidad Nacional Autónoma de México, Querétaro, México
| | - Brittany L. Mitchell
- Mental Health and Neuroscience Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia
| | - Alejandra Medina-Rivera
- Laboratorio Internacional de Investigación Sobre el Genoma Humano, Universidad Nacional Autónoma de México, Juriquilla, Querétaro, México
| | - Miguel E. Rentería
- Mental Health and Neuroscience Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia
- School of Biomedical Sciences, Faculty of Medicine, University of Queensland, Brisbane, QLD, Australia
- School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane, QLD,Australia
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Morbidity and Associated Factors of Depressive Disorder in Patients With Parkinson's Disease. J Nerv Ment Dis 2022; 210:777-783. [PMID: 35687726 DOI: 10.1097/nmd.0000000000001537] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
Parkinson's disease (PD) is a progressive, neurodegenerative disorder and is commonly comorbid with depression. The aim of this cross-sectional study was to assess morbidity and associated factors of depression in patients with PD. In total, 181 patients with PD were enrolled and assessed using the Mini-International Neuropsychiatric Interview. Of the sample, 51% had at least one psychiatric diagnosis. The most prevalent psychiatric disorder was depressive disorder (27.6%), followed by rapid eye movement sleep behavior disorder (9.9%), insomnia disorder (8.8%), and adjustment disorder (2.8%). Severity of anxiety, suicide risk, and anxiolytics/hypnotics use were factors associated with depressive disorder in PD patients. Furthermore, severity of anxiety was significantly linked with suicide risk. We suggest that use of a standardized structured interview for early detection of depression in PD patients is crucial. Anxiety, anxiolytics/hypnotics use, depression, and suicide risks are interrelated and warrant clinical concerns regarding PD patients.
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Bougea A, Stefanis L, Chrousos G. Stress system and related biomarkers in Parkinson's disease. Adv Clin Chem 2022; 111:177-215. [DOI: 10.1016/bs.acc.2022.07.004] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/15/2022]
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Gibson LL, Pollak TA, Heslegrave A, Hye A, Batzu L, Rota S, Trivedi D, Nicholson TR, Ffytche D, Zetterberg H, Chaudhuri KR, Aarsland D. Plasma Neurofilament Light and p-tau181 and Risk of Psychosis in Parkinson's Disease. JOURNAL OF PARKINSON'S DISEASE 2022; 12:1527-1538. [PMID: 35466956 PMCID: PMC7616984 DOI: 10.3233/jpd-223182] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 06/14/2023]
Abstract
BACKGROUND Neuropsychiatric symptoms are common and important to people with Parkinson's disease (PD), but their etiology is poorly understood. Plasma neurofilament light (NfL) and p-tau181 are biomarkers of neuro-axonal degeneration and tau pathology respectively, which have yet to be explored in association with the affective and psychotic symptoms in PD. OBJECTIVE To investigate the relationship between plasma NfL and p-tau181 with the affective and psychotic symptoms in PD. METHODS We assessed the baseline concentration of plasma NfL and p-tau181 in a cohort of 108 patients with PD and 38 healthy controls. A subgroup of patients (n = 63) were assessed annually with clinical measures for up to 7 years. Psychotic symptoms were assessed using the Non-Motor Symptom Scale and affective symptoms were measured in the Hospital Anxiety and Depression Scale. RESULTS Baseline plasma NfL was a significant predictor of psychotic symptoms longitudinally across the study adjusted for age, Hoehn and Yahr stage, duration of follow up, duration of disease, baseline levodopa and dopamine agonist medication, and baseline cognition: (OR 8.15 [95% CI 1.40-47.4], p = 0.020). There was no association between NfL concentration and the cumulative prevalence of affective symptoms. Plasma p-tau181 concentration was not associated with psychotic or affective symptoms. CONCLUSION These findings suggest psychotic symptoms are associated with greater neurodegeneration in PD. Further studies are needed to explore NfL as a potential biomarker for psychosis in PD.
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Affiliation(s)
- Lucy L Gibson
- Old Age Psychiatry Department, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK
| | - Thomas A Pollak
- Neuropsychiatry Research and Education Group, Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK
| | - Amanda Heslegrave
- Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK
- UK Dementia Research Institute at UCL, London, UK
| | - Abdul Hye
- Old Age Psychiatry Department, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK
| | - Lucia Batzu
- Department of Basic and Clinical Neuroscience, Parkinson Foundation International Centre of Excellence, Kings College Hospital and Kings College London, London, UK
| | - Silvia Rota
- Department of Basic and Clinical Neuroscience, Parkinson Foundation International Centre of Excellence, Kings College Hospital and Kings College London, London, UK
| | - Dhaval Trivedi
- Department of Basic and Clinical Neuroscience, Parkinson Foundation International Centre of Excellence, Kings College Hospital and Kings College London, London, UK
| | - Timothy R Nicholson
- Neuropsychiatry Research and Education Group, Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK
| | - Dominic Ffytche
- Old Age Psychiatry Department, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK
| | - Henrik Zetterberg
- Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK
- UK Dementia Research Institute at UCL, London, UK
- Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden
- Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Salhgrenska Academy at the University of Gothenburg, Gothenburg, Sweden
- Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China
| | - K Ray Chaudhuri
- Department of Basic and Clinical Neuroscience, Parkinson Foundation International Centre of Excellence, Kings College Hospital and Kings College London, London, UK
| | - Dag Aarsland
- Old Age Psychiatry Department, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK
- Centre for Age-Related Disease, Stavanger University Hospital, Stavanger, Norway
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Insights into the Pathophysiology of Psychiatric Symptoms in Central Nervous System Disorders: Implications for Early and Differential Diagnosis. Int J Mol Sci 2021; 22:ijms22094440. [PMID: 33922780 PMCID: PMC8123079 DOI: 10.3390/ijms22094440] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/26/2021] [Revised: 04/16/2021] [Accepted: 04/21/2021] [Indexed: 12/12/2022] Open
Abstract
Different psychopathological manifestations, such as affective, psychotic, obsessive-compulsive symptoms, and impulse control disturbances, may occur in most central nervous system (CNS) disorders including neurodegenerative and neuroinflammatory diseases. Psychiatric symptoms often represent the clinical onset of such disorders, thus potentially leading to misdiagnosis, delay in treatment, and a worse outcome. In this review, psychiatric symptoms observed along the course of several neurological diseases, namely Alzheimer’s disease, fronto-temporal dementia, Parkinson’s disease, Huntington’s disease, and multiple sclerosis, are discussed, as well as the involved brain circuits and molecular/synaptic alterations. Special attention has been paid to the emerging role of fluid biomarkers in early detection of these neurodegenerative diseases. The frequent occurrence of psychiatric symptoms in neurological diseases, even as the first clinical manifestations, should prompt neurologists and psychiatrists to share a common clinico-biological background and a coordinated diagnostic approach.
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Zečević I. Clinical practice guidelines based on evidence for cognitive-behavioural therapy in Parkinson's disease comorbidities: A literature review. Clin Psychol Psychother 2020; 27:504-514. [PMID: 32196842 DOI: 10.1002/cpp.2448] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/29/2020] [Revised: 03/17/2020] [Accepted: 03/17/2020] [Indexed: 12/18/2022]
Abstract
The purpose of this review is to provide psychologists and other health care professional enough knowledge about available cognitive-behavioural interventions for comorbidities in Parkinson's disease that include depression, anxiety, impulsive disorder, pain, and sleep disturbances. This review has clear clinical practical suggestions how to adapt psychological interventions and techniques to the motor and/or cognitive impairments of patients with Parkinson's disease, based on earlier available research results. Every available research that could be found with the help of search engines from Medline, Springer, PsychINFO, and Google Scholar, which used cognitive-behavioural therapy to treat Parkinson's comorbidities, was cited and explained. Cognitive-behavioural interventions and techniques are presented based on available research results for Parkinson's comorbidities. It is recommended to use treatment plans and interventions that are earlier suggested as efficient in patients with Parkinson's disease. Strongest available research based recommendations are available for depression and anxiety. There are only few available research studies that used cognitive and/or behavioural interventions for pain, impulsive disorder, or sleeping disturbances, except insomnia in Parkinson's disease. Cognitive-behavioural therapy is safe to use and should be adapted to the specific needs of patients and with the scientific approved treatment interventions and techniques. Psychologists should be careful on how they adapt their treatment plan for patients.
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Affiliation(s)
- Ivan Zečević
- Department of Psychosocial Rehabilitation, Center for Rehabilitation Stančić, Zagreb, Croatia
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van Wamelen DJ, Wan YM, Ray Chaudhuri K, Jenner P. Stress and cortisol in Parkinson's disease. INTERNATIONAL REVIEW OF NEUROBIOLOGY 2020; 152:131-156. [PMID: 32450994 DOI: 10.1016/bs.irn.2020.01.005] [Citation(s) in RCA: 19] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Stress is ubiquitous with many factors contributing to its effects, including psychological responses and associated biological factors, including cortisol related physiological responses, and inflammation. Also in Parkinson's disease there is growing evidence for the role of stress in some key symptoms, even stretching to the prodromal stage. Here we discuss the possible contributions of the range and nature of stress in PD and we aim to summarize the current knowledge about the role of stress-related responses on motor and non-motor symptoms, the underlying pathophysiology, and the potential implications for treatment.
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Affiliation(s)
- Daniel J van Wamelen
- King's College London, Department of Neurosciences, Institute of Psychiatry, Psychology & Neuroscience, London, United Kingdom; Parkinson Foundation Centre of Excellence, King's College Hospital, London, United Kingdom.
| | - Yi-Min Wan
- King's College London, Department of Neurosciences, Institute of Psychiatry, Psychology & Neuroscience, London, United Kingdom; Parkinson Foundation Centre of Excellence, King's College Hospital, London, United Kingdom; Department of Psychiatry, Ng Teng Fong General Hospital, Singapore, Singapore
| | - K Ray Chaudhuri
- King's College London, Department of Neurosciences, Institute of Psychiatry, Psychology & Neuroscience, London, United Kingdom; Parkinson Foundation Centre of Excellence, King's College Hospital, London, United Kingdom
| | - Peter Jenner
- King's College London, Neurodegenerative Diseases Research Group, Institute of Pharmaceutical Sciences, Faculty of Health Sciences and Medicine, London, United Kingdom
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Milyukhina IV. Pathogenesis, clinical features, and treatments of depression in Parkinson's disease. NEUROLOGY, NEUROPSYCHIATRY, PSYCHOSOMATICS 2019. [DOI: 10.14412/2074-2711-2019-2-93-99] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/03/2022]
Abstract
Depression is the most common non-motor manifestation of Parkinson's disease (PD), which significantly affects the rate of disease progression and increases the risk of motor complications and dementia. The paper considers the etiology and pathogenesis, cause-and-effect factors of depression in PD, and features of its diagnosis and treatment. Attention is paid to the algorithm for a physician's actions in the detection of depressive disorder in a patient with PD, to the choice of an antidepressant, and to the promising areas of therapy.
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Affiliation(s)
- I. V. Milyukhina
- Institute of Experimental Medicine;
Acad. I.P. Pavlov First Saint Petersburg State Medical University, Ministry of Health of Russia
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Rudyk C, Dwyer Z, McNeill J, Salmaso N, Farmer K, Prowse N, Hayley S. Chronic unpredictable stress influenced the behavioral but not the neurodegenerative impact of paraquat. Neurobiol Stress 2019; 11:100179. [PMID: 31304199 PMCID: PMC6599913 DOI: 10.1016/j.ynstr.2019.100179] [Citation(s) in RCA: 21] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2019] [Revised: 05/03/2019] [Accepted: 05/30/2019] [Indexed: 01/09/2023] Open
Abstract
The impact of psychological stressors on the progression of motor and non-motor disturbances observed in Parkinson's disease (PD) has received little attention. Given that PD likely results from many different environmental “hits”, we were interested in whether a chronic unpredictable stressor regimen would act additively or possibly even synergistically to augment the impact of the toxicant, paraquat, which has previously been linked to PD. Our findings support the contention that paraquat itself acted as a systemic stressor, with the pesticide increasing plasma corticosterone, as well as altering glucocorticoid receptor (GR) expression in the hippocampus. Furthermore, stressed mice that also received paraquat displayed synergistic motor coordination impairment on a rotarod test and augmented signs of anhedonia (sucrose preference test). The individual stressor and paraquat treatments also caused a range of non-motor (e.g. open field, Y and plus mazes) deficits, but there were no signs of an interaction (neither additive nor synergistic) between the insults. Similarly, paraquat caused the expected loss of substantia nigra dopamine neurons and microglial activation, but this effect was not further influenced by the chronic stressor. Taken together, these results indicate that paraquat has many effects comparable to that of a more traditional stressor and that at least some behavioral measures (i.e. sucrose preference and rotarod) are augmented by the combined pesticide and stress treatments. Thus, although psychological stressors might not necessarily increase the neurodegenerative effects of the toxicant exposure, they may promote co-morbid behaviors pathology.
Paraquat induced behavioral and neurochemical alterations similar to those induced by a chronic unpredictable stressor. Chronic unpredictable stress did not influence the degeneration of midbrain dopamine neurons or microglia activation. The paraquat and chronic stressor exposure resulted in augmented motor impairment and anhedonic-like behavior.
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Key Words
- AAR, alternate arm return
- ANOVA, analysis of variance
- BCA, bicinchoninic acid
- BDNF, brain derived neurotrophic factor
- CUS, chronic unpredictable stress
- Cytokine
- EDTA, ethylenediaminetetraacetic acid
- ELISA, enzyme-linked immunosorbent assay
- EPM, elevated plus maze
- FST, forced swim test
- GR, glucocorticoid receptor
- HPA, hypothalamus-pituitary adrenal
- IBA1, ionized calcium-binding adapter molecule 1
- Inflammatory
- MMx, Micromax
- Microglia
- PB, phosphate buffer
- PBS, phosphate buffered saline
- PD, Parkinson's disease
- PFA, paraformaldehyde
- PVDF, polyvinylidene difluoride
- Parkinson's
- RIPA, Radio Immuno Precipitation Assay
- RR, rotarod
- SAB, spontaneous alternation behavior
- SAR, same arm return
- SDS, sodium dodecyl sulphate
- SNc, substantia nigra pars compacta
- SPT, sucrose preference test
- Stress
- TH, tyrosine hydroxylase
- Toxicity
- VTA, ventral tegmental area
- pGR, phosphate glucocorticoid receptor
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Affiliation(s)
- Chris Rudyk
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada, K1S 5B6
| | - Zach Dwyer
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada, K1S 5B6
| | - Jessica McNeill
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada, K1S 5B6
| | - Natalina Salmaso
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada, K1S 5B6
| | - Kyle Farmer
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada, K1S 5B6.,Department of Neurology, University of Pittsburgh, Pittsburgh, PA, 15213, USA
| | - Natalie Prowse
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada, K1S 5B6
| | - Shawn Hayley
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada, K1S 5B6
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Valcarenghi RV, Alvarez AM, Santos SSC, Siewert JS, Nunes SFL, Tomasi AVR. The daily lives of people with Parkinson's disease. Rev Bras Enferm 2018; 71:272-279. [PMID: 29412283 DOI: 10.1590/0034-7167-2016-0577] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/23/2016] [Accepted: 04/11/2017] [Indexed: 11/22/2022] Open
Abstract
OBJECTIVE To understand the daily lives of people with Parkinson's disease. METHOD Qualitative research, using as methodological and theoretical referential the Grounded Theory and Symbolic Interactionism, respectively. The in-depth interview was conducted with 30 people with Parkinson's disease. RESULTS From data analysis, three themes were selected: Living with the disease - living with the treatment and changes in lifestyle; Modifying of one's job performance - revealing incapacity for work and the need to anticipate retirement and; Living with the stigma - the feeling of prejudice against the disease and the perceived limitations of the health services. FINAL CONSIDERATIONS Living with a chronic and non-transferable disease encompasses social, physical and cultural effects, along with the personal experiences of each unique individual. This study assists the improvement of care to people with the disease, because the care practice emerges from the interactions between the subjects.
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Affiliation(s)
- Rafaela Vivian Valcarenghi
- Universidade Federal de Santa Catarina, Postgraduate Program in Nursing. Florianópolis, Santa Catarina, Brazil
| | - Angela Maria Alvarez
- Universidade Federal de Santa Catarina, Postgraduate Program in Nursing. Florianópolis, Santa Catarina, Brazil
| | - Silvana Sidney Costa Santos
- Universidade Federal do Rio Grande, School of Nursing, Department of Nursing. Rio Grande, Rio Grande do Sul, Brazil
| | - Josiane Steil Siewert
- Universidade Federal de Santa Catarina, Postgraduate Program in Nursing. Florianópolis, Santa Catarina, Brazil
| | | | - Andrelise Viana Rosa Tomasi
- Universidade Federal de Santa Catarina, Postgraduate Program in Nursing. Florianópolis, Santa Catarina, Brazil
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Tanguy A, Jönsson L, Ishihara L. Inventory of real world data sources in Parkinson's disease. BMC Neurol 2017; 17:213. [PMID: 29216834 PMCID: PMC5721688 DOI: 10.1186/s12883-017-0985-0] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/16/2017] [Accepted: 11/22/2017] [Indexed: 11/10/2022] Open
Abstract
Background Real world data have an important role to play in the evaluation of epidemiology and burden of disease; and in assisting health-care decision-makers, especially related to coverage and payment decisions. However, there is currently no overview of the existing longitudinal real world data sources in Parkinson’s disease (PD) in the USA. Such an assessment can be very helpful, to support a future effort to harmonize real world data collection and use the available resources in an optimal way. Methods The objective of this comprehensive literature review is to systematically identify and describe the longitudinal, real world data sources in PD in the USA, and to provide a summary of their measurements (categorized into 8 main dimensions: motor and neurological functions, cognition, psychiatry, activities of daily living, sleep, quality of life, autonomic symptoms and other). The literature search was performed using MEDLINE, EMBASE and internet key word search. Results Of the 53 data sources identified between May and August 2016, 16 were still ongoing. Current medications (81%) and comorbidities (79%) were frequently collected, in comparison to medical imaging (36%), genetic information (30%), caregiver burden (11%) and healthcare costs (2%). Many different measurements (n = 108) were performed and an interesting variability among used measurements was revealed. Conclusions Many longitudinal real world data sources on PD exist. Different types of measurements have been performed over time. To allow comparison and pooling of these multiple data sources, it will be essential to harmonize practices in terms of types of measurements.
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Affiliation(s)
- Audrey Tanguy
- Lundbeck SAS, 37-45 Quai du Président Roosevelt, CEDEX 92445, Issy-les-Moulineaux, France
| | - Linus Jönsson
- Lundbeck SAS, 37-45 Quai du Président Roosevelt, CEDEX 92445, Issy-les-Moulineaux, France
| | - Lianna Ishihara
- Lundbeck SAS, 37-45 Quai du Président Roosevelt, CEDEX 92445, Issy-les-Moulineaux, France.
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Trojano L, Papagno C. Cognitive and behavioral disorders in Parkinson's disease: an update. II: behavioral disorders. Neurol Sci 2017; 39:53-61. [PMID: 29038946 DOI: 10.1007/s10072-017-3155-7] [Citation(s) in RCA: 31] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/18/2017] [Accepted: 10/10/2017] [Indexed: 12/11/2022]
Abstract
Patients with Parkinson's disease (PD) can experience several behavioral symptoms, such as apathy, agitation, hypersexuality, stereotypic movements, pathological gambling, abuse of antiparkinsonian drugs, and REM sleep behavioral disorders. Psychoses and hallucinations, depression and anxiety disorders, and difficulties in recognizing and experiencing emotions also impair behavior and can cause severe psychosocial problems in patients with PD. Symptoms can be present since early stages of the disease, sometimes even before the appearance of classical motor symptoms, likely in relation to dopamine depletion in basal ganglia and/or to dysfunctions of other neurotrasmitter systems, and others can develop later, in some cases in relation to dopaminergic treatment. In this paper, we review recent literature, with particular attention to the last 5 years, on the main behavioral and emotional disturbances described in PD patients as well as the hypothesized neurofunctional substrate of such impairments. Finally, we provide some suggestions on the most suitable instruments to check and assess PD-associated behavioral defects over time.
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Affiliation(s)
- Luigi Trojano
- Department of Psychology, University of Campania 'Luigi Vanvitelli', Viale Ellittico 31, 81100, Caserta, Italy.
- ICS Maugeri, IRCCS, Telese Terme, Italy.
| | - Costanza Papagno
- CIMeC, University of Trento, Trento, Italy.
- Department of Psychology, University of Milano-Bicocca, Piazza dell'Ateneo 1, 02100, Milan, Italy.
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Wu Q, Yang X, Zhang Y, Zhang L, Feng L. Chronic mild stress accelerates the progression of Parkinson's disease in A53T α-synuclein transgenic mice. Exp Neurol 2016; 285:61-71. [DOI: 10.1016/j.expneurol.2016.09.004] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/30/2016] [Revised: 09/02/2016] [Accepted: 09/11/2016] [Indexed: 10/21/2022]
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Abstract
BACKGROUND Parkinson's disease (PD) has a major impact on mobility, as well as cognition which can consequently impair aspects of individual's lives. Many studies have examined the living experiences of individuals with PD and its impact on their daily lives. None of these studies have explored the life experiences of Jordanian individuals living with PD. Therefore, the purpose of this qualitative study was to describe the daily living experiences and impact on lives of Jordanian individuals with PD. METHODS A qualitative phenomenological design was used. Interviews were recorded and transcribed. Transcripts were analysed using thematic analysis. RESULTS Experiences of 8 Jordanian individuals with PD who participated in this study can be categorized in the following major themes: (1) challenging perspectives and (2) adaptations. Challenging perspectives included stigma, emotional drainer, and experience of decreased independence and difficulty in occupational performance. Adaptations included embracing early acceptance and intervention, spiritual experience, and family support. CONCLUSIONS Study provided a wealth of knowledge related to the effect of PD and its intersection with the Arabic Jordanian culture. Such knowledge should aid healthcare professionals involved with providing services to Jordanian individuals with PD to provide better holistic services.
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Affiliation(s)
- Mohammad S Nazzal
- a Department of Rehabilitation Sciences, Faculty of Applied Medical Sciences , Jordan University of Science and Technology , Irbid , Jordan
| | - Hanan Khalil
- a Department of Rehabilitation Sciences, Faculty of Applied Medical Sciences , Jordan University of Science and Technology , Irbid , Jordan
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Schwartz R, Pell MD. When emotion and expression diverge: The social costs of Parkinson’s disease. J Clin Exp Neuropsychol 2016; 39:211-230. [DOI: 10.1080/13803395.2016.1216090] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
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17
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Wolter DK. Depressionen im höheren Lebensalter, Teil 2. Z Gerontol Geriatr 2016; 49:437-52. [DOI: 10.1007/s00391-016-1022-4] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/06/2015] [Accepted: 11/11/2015] [Indexed: 11/28/2022]
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Rudyk C, Litteljohn D, Syed S, Dwyer Z, Hayley S. Paraquat and psychological stressor interactions as pertains to Parkinsonian co-morbidity. Neurobiol Stress 2015; 2:85-93. [PMID: 26844243 PMCID: PMC4730791 DOI: 10.1016/j.ynstr.2015.09.001] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/12/2015] [Accepted: 09/12/2015] [Indexed: 02/08/2023] Open
Abstract
A number of epidemiological and experimental studies have implicated the non-selective herbicide, paraquat, in the development of sporadic Parkinson's disease (PD). While preclinical research has focused mainly on elucidating the nigrostriatal effects of paraquat, relatively little data are available concerning non-motor brain systems and inflammatory immune processes (which have been implicated in PD). Hence, in the present study, we sought to take a multi-system approach to characterize the influence of paraquat upon extra-nigrostriatal brain regions, as well ascertain whether the impact of the pesticide might be enhanced in the context of chronic intermittent stressor exposure. Our findings support the contention that paraquat itself acted as a systemic stressor, with the pesticide increasing plasma corticosterone, as well as altering neurochemical activity in the locus coeruleus, paraventricular nucleus of the hypothalamus, nucleus accumbens, dorsal striatum, and central amygdala. However, with the important exception striatal dopamine turnover, the stressor treatment did not further augment these effects. Additionally, paraquat altered inter-cytokine correlations and, to a lesser extent, circulating cytokine levels, and concomitant stress exposure modulated some of these effects. Finally, paraquat provoked significant (albeit modest) reductions of sucrose preference and weight gain, hinting at possible anhendonic-like or sickness responses. These data suggest that, in addition to being a well known oxidative stress generator, paraquat can act as a systemic stressor affecting hormonal and neurochemical activity, but largely not interacting with a concomitant stressor regimen.
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Key Words
- 5-HIAA, 5-hydroxyindole acetic acid
- 5-HT, serotonin
- ANOVA, analysis of variance
- Anhedonia
- CIS, chronic intermittent immobilization/social defeat stressor
- Cytokine
- DA, dopamine
- DOPAC, 3,4-Dihydroxyphenylacetic acid
- EDTA, ethylenediaminetetraacetic acid
- GM-CSF, granulocyte-macrophage colony-stimulating factor
- HPLC, high-performance liquid chromatography
- HVA, homovanillic acid
- IFN-γ, interferon-γ
- IL, interleukin
- KO, knockout
- LC, locus coeruleus
- LLOQ, lower limit of quantification
- MCP, monocyte chemoatrractant protein
- MHPG, 3-methoxy-4-hydroexyphenylglycol
- MIP, macrophage inflammatory protein
- Monoamine
- NE, norepinephrine
- Neuroendocrine
- PD, Parkinson's disease
- PVN, paraventricular nucleus
- Pesticide
- Stressor
- TNF-α, tumour necrosis factor-alpha
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Affiliation(s)
- Chris Rudyk
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada
| | - Darcy Litteljohn
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada
| | - Shuaib Syed
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada
| | - Zach Dwyer
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada
| | - Shawn Hayley
- Department of Neuroscience, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada
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19
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Hsu YT, Liao CC, Chang SN, Yang YW, Tsai CH, Chen TL, Sung FC. Increased Risk of Depression in Patients with Parkinson Disease: A Nationwide Cohort Study. Am J Geriatr Psychiatry 2015; 23:934-40. [PMID: 25529799 DOI: 10.1016/j.jagp.2014.10.011] [Citation(s) in RCA: 32] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/24/2014] [Revised: 10/20/2014] [Accepted: 10/30/2014] [Indexed: 11/24/2022]
Abstract
OBJECTIVE The association between Parkinson disease (PD) and depression remains unclear, particularly in the Asian population. The purpose of this study is to investigate the risk of depression in patients with PD using population-based data. METHODS Based on the National Health Insurance Research Database of Taiwan, we identified 1,698 patients with PD aged 40 years or older diagnosed in 2000-2003. With frequency matching procedure, we randomly selected 6,792 subjects without PD stratified by sex and age. Both cohorts were followed until the end of 2008 or diagnosis of depression. Risk of depression associated with PD was estimated in the multivariate Cox hazards regressions. Diabetes, hypertension, and hyperlipidemia were more prevalent at baseline in patients with PD. RESULTS Compared with the cohort without PD, the hazard ratio (HR) for depression in PD patients was 4.06 (95% CI: 3.15-5.23), which increased to 4.26 (95% CI: 3.29-5.51) after adjustment for age, sex, urbanization, income, and coexisting medical conditions. In the sex stratification, the HR of depression for men with PD was 4.42 (95% CI: 2.93-6.67) compared with men without PD. The HR for the association between PD and depression in women was 4.22 (95% CI: 3.02-5.88). CONCLUSION This study suggests that patients with PD are at an elevated risk of depression, particularly for men. Integrated care for early identification and treatment of depression are crucial for patients with PD.
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Affiliation(s)
- Yi-Ting Hsu
- Neuroscience Laboratory, Department of Neurology, China Medical University Hospital, Taichung, Taiwan; School of Medicine, China Medical University, Taichung, Taiwan
| | - Chien-Chang Liao
- Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan; School of Chinese Medicine, China Medical University, Taichung, Taiwan; Department of Anesthesiology, Taipei Medical University Hospital, Taipei, Taiwan; School of Medicine, Taipei Medical University, Taipei, Taiwan
| | - Shih-Ni Chang
- Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan
| | - Yu-Wan Yang
- Neuroscience Laboratory, Department of Neurology, China Medical University Hospital, Taichung, Taiwan; School of Medicine, China Medical University, Taichung, Taiwan
| | - Chon-Haw Tsai
- Neuroscience Laboratory, Department of Neurology, China Medical University Hospital, Taichung, Taiwan; School of Medicine, China Medical University, Taichung, Taiwan
| | - Ta-Liang Chen
- Department of Anesthesiology, Taipei Medical University Hospital, Taipei, Taiwan; School of Medicine, Taipei Medical University, Taipei, Taiwan
| | - Fung-Chang Sung
- Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan; Department of Public Health, China Medical University, Taichung, Taiwan.
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20
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Löffler LAK, Radke S, Morawetz C, Derntl B. Emotional dysfunctions in neurodegenerative diseases. J Comp Neurol 2015; 524:1727-43. [PMID: 26011035 DOI: 10.1002/cne.23816] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/30/2015] [Revised: 05/06/2015] [Accepted: 05/18/2015] [Indexed: 01/31/2023]
Abstract
Neurodegenerative diseases are characterized primarily by motor signs but are also accompanied by emotional disturbances. Because of the limited knowledge about these dysfunctions, this Review provides an overview of emotional competencies in Huntington's disease (HD), Parkinson's disease (PD), and multiple sclerosis (MS), with a focus on emotion recognition, emotion regulation, and depression. Most studies indicate facial emotion recognition deficits in HD and PD, whereas data for MS are inconsistent. On a neural level, dysfunctions of amygdala and striatum, among others, have been linked to these impairments. These dysfunctions also tap brain regions that are part of the emotion regulation network, suggesting problems in this competency, too. Research points to dysfunctional emotion regulation in MS, whereas findings for PD and HD are missing. The high prevalence of depression in all three disorders emphasizes the need for effective therapies. Research on emotional disturbances might improve treatment, thereby increasing patients' and caregivers' well-being.
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Affiliation(s)
- Leonie A K Löffler
- Department of Psychiatry, Psychotherapy and Psychosomatics, Medical Faculty, RWTH Aachen, 52074, Aachen, Germany
| | - Sina Radke
- Department of Psychiatry, Psychotherapy and Psychosomatics, Medical Faculty, RWTH Aachen, 52074, Aachen, Germany.,JARA-Translational Brain Medicine, 52074, Aachen, Germany
| | - Carmen Morawetz
- Department of Education and Psychology, Freie Universität Berlin, 14195, Berlin, Germany
| | - Birgit Derntl
- Department of Psychiatry, Psychotherapy and Psychosomatics, Medical Faculty, RWTH Aachen, 52074, Aachen, Germany.,JARA-Translational Brain Medicine, 52074, Aachen, Germany.,Institute for Neuroscience and Medicine (INM-1), Research Center Jülich, 52425, Jülich, Germany
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21
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Abdel-Salam OME. Prevalence, clinical features and treatment of depression in Parkinson’s disease: An update. World J Neurol 2015; 5:17. [DOI: 10.5316/wjn.v5.i1.17] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/28/2014] [Revised: 01/10/2015] [Accepted: 02/09/2015] [Indexed: 02/06/2023] Open
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22
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Affiliation(s)
- A H V Schapira
- Department of Clinical Neurosciences, UCL Institute of Neurology, London, UK.
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23
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Schapira AHV. The measurement and importance of non-motor symptoms in Parkinson disease. Eur J Neurol 2014; 22:2-3. [DOI: 10.1111/ene.12523] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
Affiliation(s)
- A. H. V. Schapira
- Department of Clinical Neurosciences; UCL Institute of Neurology; London UK
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24
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Abstract
Depressive disturbances are common in patients with Parkinson's disease (PD) and influence many other clinical aspects of the disease. In addition to causing inherent emotional distress, depressive disorders negatively impact quality of life, motor and cognitive deficits, functional disability, and other psychiatric comorbidities in patients with PD. Knowledge of the pathophysiology of PD depression remains limited. However, clinical studies demonstrate the efficacy of medications and psychotherapies for PD depression, underscoring the importance of their timely detection and concerted management.
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25
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Leentjens AFG, Moonen AJH, Dujardin K, Marsh L, Martinez-Martin P, Richard IH, Starkstein SE, Köhler S. Modeling depression in Parkinson disease: disease-specific and nonspecific risk factors. Neurology 2013; 81:1036-43. [PMID: 23946309 DOI: 10.1212/wnl.0b013e3182a4a503] [Citation(s) in RCA: 46] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022] Open
Abstract
OBJECTIVE To construct a model for depression in Parkinson disease (PD) and to study the relative contribution of PD-specific and nonspecific risk factors to this model. METHODS Structural equation modeling of direct and indirect associations of risk factors with the latent depression outcome using a cross-sectional dataset of 342 patients with PD. RESULTS A model with acceptable fit was generated that explained 41% of the variance in depression. In the final model, 3 PD-specific variables (increased disease duration, more severe motor symptoms, the use of levodopa) and 6 nonspecific variables (female sex, history of anxiety and/or depression, family history of depression, worse functioning on activities of daily living, and worse cognitive status) were maintained and significantly associated with depression. Nonspecific risk factors had a 3-times-higher influence in the model than PD-specific risk factors. CONCLUSION In this cross-sectional study, we showed that nonspecific factors may be more prominent markers of depression than PD-specific factors. Accordingly, research on depression in PD should focus not only on factors associated with or specific for PD, but should also examine a wider scope of factors including general risk factors for depression, not specific for PD.
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Affiliation(s)
- Albert F G Leentjens
- From the Department of Psychiatry (A.F.G.L., A.J.H.M.), Maastricht University Medical Center, Maastricht; School for Mental Health and Neuroscience (A.F.G.L., A.J.H.M., S.K.), Maastricht University, Maastricht, the Netherlands; Neurology and Movement Disorders Unit (K.D.), Lille University Medical Center, Lille, France; Mental Health Care Line (L.M.), Michael E. DeBakey Veterans Administration Medical Center and Departments of Psychiatry and Neurology, Baylor College of Medicine, Houston, TX; Alzheimer Disease Research Unit and CIBERNED (P.M.-M.), Alzheimer Center Reina Sofia Foundation, Carlos III Institute of Health, Madrid, Spain; Departments of Neurology and Psychiatry (I.H.R.), University of Rochester School of Medicine and Dentistry, Rochester, NY; and School of Psychiatry (S.E.S.), University of Western Australia and Fremantle Hospital, Fremantle, Australia
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