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Parkinson's disease
Open accessAbstract
Parkinson's disease is a recognisable clinical syndrome with a range of causes and clinical presentations. Parkinson's disease represents a fast-growing neurodegenerative condition; the rising prevalence worldwide resembles the many characteristics typically observed during a pandemic, except for an infectious cause. In most populations, 3-5% of Parkinson's disease is explained by genetic causes linked to known Parkinson's disease genes, thus representing monogenic Parkinson's disease, whereas 90 genetic risk variants collectively explain 16-36% of the heritable risk of non-monogenic Parkinson's disease. Additional causal associations include having a relative with Parkinson's disease or tremor, constipation, and being a non-smoker, each at least doubling the risk of Parkinson's disease. The diagnosis is clinically based; ancillary testing is reserved for people with an atypical presentation. Current criteria define Parkinson's disease as the presence of bradykinesia combined with either rest tremor, rigidity, or both. However, the clinical presentation is multifaceted and includes many non-motor symptoms. Prognostic counselling is guided by awareness of disease subtypes. Clinically manifest Parkinson's disease is preceded by a potentially long prodromal period. Presently, establishment of prodromal symptoms has no clinical implications other than symptom suppression, although recognition of prodromal parkinsonism will probably have consequences when disease-modifying treatments become available. Treatment goals vary from person to person, emphasising the need for personalised management. There is no reason to postpone symptomatic treatment in people developing disability due to Parkinson's disease. Levodopa is the most common medication used as first-line therapy. Optimal management should start at diagnosis and requires a multidisciplinary team approach, including a growing repertoire of non-pharmacological interventions. At present, no therapy can slow down or arrest the progression of Parkinson's disease, but informed by new insights in genetic causes and mechanisms of neuronal death, several promising strategies are being tested for disease-modifying potential. With the perspective of people with Parkinson's disease as a so-called red thread throughout this Seminar, we will show how personalised management of Parkinson's disease can be optimised.
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“Strikingly, non-motor symptoms remain poorly responsive to current PD treatments despite being present from early prodromal PD and contributing significantly to overall disease burden [36].”
From The gut–brain axis in early Parkinson’s disease: from prodrome to prevention (2025) · cites this paper as [36]
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“Clinical practice guidelines support resilience training and exercise for patients with Parkinson’s disease (PD).”
From A randomized clinical trial of mindfulness meditation versus exercise in Parkinson’s disease during social unrest (2023) · cites this paper as [1]
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“The diseases encompass various severe conditions, including neurodegenerative disorders like Alzheimer’s disease (AD) [3, 4] and Parkinson’s disease (PD) [5, 6], as well as traumatic brain injuries (TBI) [7] and spinal cord injuries (SCI) [8].”
From Extracellular vesicles as nanotheranostic platforms for targeted neurological disorder interventions (2024) · cites this paper as [5]
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Training dual tasks together or apart in Parkinson's disease: Results from the DUALITY trial
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Smartphone motor testing to distinguish idiopathic REM sleep behavior disorder, controls, and PD
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COVID ‐19 in Parkinson’s Disease Patients Living in Lombardy, Italy
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Biological and Clinical Implications of Comorbidities in Parkinson’s Disease
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Self-citationCSF or Serum Neurofilament Light Added to α‐Synuclein Panel Discriminates Parkinson's From Controls
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Cognitive training for freezing of gait in Parkinson’s disease: a randomized controlled trial
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On behalf of the CPN study group, Eggers, C., Dano, R., Schill, J., Fink, G. R., Hellmich, M., & Timmermann, L. (2018) · Journal of Neurology · doi:10.1007/s00415-018-8761-7 · Cited by 85
Frequency of Loss of Function Variants in LRRK2 in Parkinson Disease
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Bright light therapy for depression in Parkinson disease: A randomized controlled trial
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β-adrenoreceptors and the risk of Parkinson's disease
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The Parkinson's Disease Mendelian Randomization Research Portal
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Neurological diseases and risk of suicide attempt: a case–control study
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Defining Palliative Care Needs in Parkinson's Disease
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PINK1-dependent mitophagy is driven by the UPS and can occur independently of LC3 conversion
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Randomized trial of care management to improve Parkinson disease care quality
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GBA1-associated parkinsonism: new insights and therapeutic opportunities
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Plasma urate and risk of Parkinson's disease: A mendelian randomization study
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Focused ultrasound thalamotomy in Parkinson disease
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Underrepresentation of women in Parkinson's disease trials
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Self-citationLoss of independence in early Parkinson disease
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Screening of Parkinsonian subtle fine-motor impairment from touchscreen typing via deep learning
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Precision Medicine in Parkinson’s Disease – Exploring Patient-Initiated Self-Tracking
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Self-citationUsing global team science to identify genetic parkinson's disease worldwide
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Clinical correlates of cerebral white matter abnormalities in patients with Parkinson's disease
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Office-Based Screening for Dementia in Parkinson Disease
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Survival rates among Parkinson's disease patients who carry mutations in the LRRK2 and GBA genes
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The Linked Clinical Trials initiative ( LCT ) for Parkinson's disease
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Professional occupation and the risk of Parkinson's disease
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Self-citationOptimizing Treatment in Undertreated Late-Stage Parkinsonism: A Pragmatic Randomized Trial
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Self-citationLevodopa response in later stages of Parkinson's disease: A case-control study
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MRIgFUS in tremor-dominant PD does not lead to substantial cognitive adverse events
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Metadata
- Authors
- Bloem, B. R., Okun, M. S., & Klein, C.
- Affiliations
- Radboud University Nijmegen (NL)
- University of Florida Health (US)
- University Hospital Schleswig-Holstein (DE)
- Corresponding author
- Bloem, Bastiaan R
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2021-06
- Volume
- 397
- Issue
- 10291
- Pages
- 2284-2303
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- OpenAlex
- W4206481149
- Cited by
- 3,920
- References
- 159
- Citations by year
- 2026: 878 · 2025: 1098 · 2024: 901 · 2023: 607 · 2022: 364 · 2021: 72
- FWCI
- 62.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion, other-oa)
- Funders
- Deutsche Forschungsgemeinschaft
- Parkinson's Foundation (FOR2488)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Clinical Neurology › Deep Brain Stimulation and Movement Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, neurodegeneration, genetic risk variants, monogenic Parkinson's disease, non-motor symptoms, levodopa, disease-modifying therapy, multidisciplinary care, non-pharmacological treatment, diagnosis, prodromal period
- MeSH terms
- Antiparkinson Agents, Humans, Levodopa, Parkinson Disease, Time Factors, Tremor, Disease Management, Prodromal Symptoms
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