ArticleThe Journal of clinical investigation2011
Intra-neuronal vesicular uptake of catecholamines is decreased in patients with Lewy body diseases.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Cerebrospinal fluid biomarkers for diagnosis of Parkinson's disease: a systematic review and network meta-analysis.Journal of neurology · 2025Pooled it
- Relationship between Parkinson's disease and cardio-cerebrovascular diseases: a Mendelian randomized study.Scientific reports · 2023Trial
- Catecholamine metabolism revisited: from neurochemistry to integrative physiology and pathophysiology.Physiological reviews · 2026Review
- Preclinical Catecholaminergic Biomarkers of Central Lewy Body Diseases.Journal of clinical neurology (Seoul, Korea) · 2026Review
- Multitracer PET to Assess Cardiac Sympathetic Innervation and Vesicular Storage in Lewy Body Diseases.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- Decreased urinary excretion of norepinephrine and dopamine in autonomic synucleinopathies.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Article
- Synaptic sabotage: How Tau and α-Synuclein undermine synaptic health.The Journal of cell biology · 2025Review
- Dopamine transporter and synaptic vesicle sorting defects underlie auxilin-associated Parkinson's disease.Cell reports · 2023Article
- Modeling the Progression of Cardiac Catecholamine Deficiency in Lewy Body Diseases.Journal of the American Heart Association · 2022Article
- Assessment of myocardial sympathetic innervation with 18F-FDOPA-PET/CT in patients with autonomic dysfunction: feasibility study in IPD patients.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2022Article
- What new can we learn from cardiac sympathetic neuroimaging in synucleinopathies?Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2022Article
- Dynamic planar scintigraphy for the rapid kinetic measurement of myocardialEJNMMI research · 2021Article
- The Impact ofLife (Basel, Switzerland) · 2021Review
- Could Small Heat Shock Protein HSP27 Be a First-Line Target for Preventing Protein Aggregation in Parkinson's Disease?International journal of molecular sciences · 2021Review
- Cardioselective peripheral noradrenergic deficiency in Lewy body synucleinopathies.Annals of clinical and translational neurology · 2020Article
- "Sick-but-not-dead": multiple paths to catecholamine deficiency in Lewy body diseases.Stress (Amsterdam, Netherlands) · 2020Review
- The "Sick-but-not-Dead" Phenomenon Applied to Catecholamine Deficiency in Neurodegenerative Diseases.Seminars in neurology · 2020Review
- Cardiac sympathetic innervation and vesicular storage in pure autonomic failure.Annals of clinical and translational neurology · 2020Article
- [Molecular imaging and biology · 2020Article
- Sympathetic nervous activity and hemoglobin levels in de novo Parkinson's disease.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Several neurodegenerative disorders, including Parkinson disease (PD), are characterized by the presence of Lewy bodies - cytoplasmic inclusions containing α-synuclein protein aggregates - in the affected neurons. A poorly understood feature of Lewy body diseases is loss of sympathetic nerves in the heart and other organs, manifesting as orthostatic hypotension (OH; also known as postural hypotension). We asked whether sympathetic denervation is associated with decreased uptake of catecholamines, such as dopamine and norepinephrine, into storage vesicles within sympathetic neurons. We used 6-[18F]-dopamine (18F-DA) to track myocardial uptake and retention of catecholamines. Concurrently, the fate of intra-neuronal 18F-DA was followed by assessment of arterial plasma levels of the 18F-DA metabolite 18F-dihydroxyphenylacetic acid (18F-DOPAC). The ratio of myocardial 18F-DA to arterial 18F-DOPAC provided an index of vesicular uptake. Tracer concentrations were measured in patients with PD with or without orthostatic hypotension (PD+OH, PD-No-OH); in patients with pure autonomic failure (PAF, a Lewy body disease without parkinsonism); in patients with multiple system atrophy (MSA, a non-Lewy body synucleinopathy); and in normal controls. Patients with PD+OH or PAF had decreased vesicular 18F-DA uptake and accelerated 18F-DA loss, compared with MSA and control subjects. PD-No-OH patients could be subtyped into one of these categories based on their initial 18F-DA uptake. We conclude that sympathetic denervation in Lewy body diseases is associated with decreased vesicular uptake of neuronal catecholamines, suggesting that vesicular monoamine transport is impaired. Vesicular uptake may constitute a novel target for diagnosis, treatment, and prevention.
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Registered trials
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