ArticleJournal of the American Heart Association2022
Modeling the Progression of Cardiac Catecholamine Deficiency in Lewy Body Diseases.
Article in Journal of the American Heart Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Catecholamine metabolism revisited: from neurochemistry to integrative physiology and pathophysiology.Physiological reviews · 2026Review
- Putamen dopamine synthesis, vesicular storage, and metabolism in Parkinson disease.medRxiv : the preprint server for health sciences · 2026Article
- 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
- "Body-first" dementia with Lewy bodies.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Article
- Linking the Extended Autonomic System with the Homeostat Theory: New Perspectives about Dysautonomias.Journal of personalized medicine · 2024Article
- Cardiac noradrenergic deficiency revealed by 18F-dopamine positron emission tomography identifies preclinical central Lewy body diseases.The Journal of clinical investigation · 2024Article
- Dihydroxyphenylacetaldehyde Lowering Treatment Improves Locomotor and Neurochemical Abnormalities in the Rat Rotenone Model: Relevance to the Catecholaldehyde Hypothesis for the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Background Lewy body diseases (LBDs) feature deficiency of the sympathetic neurotransmitter norepinephrine in the left ventricular myocardium and sympathetic intra-neuronal deposition of the protein alpha-synuclein (αS). LBDs therefore are autonomic synucleinopathies. Computational modeling has revealed multiple functional abnormalities in residual myocardial sympathetic noradrenergic nerves in LBDs, including decreased norepinephrine synthesis, vesicular storage, and recycling. We report an extended model that enables predictions about the progression of LBDs and effects of genetic predispositions and treatments on that progression. Methods and Results The model combines cardiac sympathetic activation with autotoxicity mediated by the dopamine metabolite 3,4-dihydroxyphenylacetaldehyde. We tested the model by its ability to predict longitudinal empirical data based on cardiac sympathetic neuroimaging, effects of genetic variations related to particular intra-neuronal reactions, treatment by monoamine oxidase inhibition to decrease 3,4-dihydroxyphenylacetaldehyde production, and post-mortem myocardial tissue contents of catecholamines and αS. The new model generated a triphasic decline in myocardial norepinephrine content. This pattern was confirmed by empirical data from serial cardiac
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.